Neurology revision - In the last minute stylee

*Due to a variety of much rarer disorders that cause Parkinsonian features

*Very variable clinical pattern \n*Affects 15-20% of those with advanced AIDS\n

*Brief episodes of impairment of consciousness\n*No aura\n*No postictal confusion\n*No awareness\n*Typically last less than 20 seconds\n*Accompanied by few or no automatisms\n**Repetitive blinking is the most common\n*Often precipitated by hyperventilation or photic stimulation\n*Typically begin during childhood or adolescence, but may persist into adulthood\n*May not be recognised in a child\n**Indication from suddenly poor school performance\n**May develop into a generalised [[tonic-clonic seizure|Tonic-clonic seizures (grand mal)]]\n

*An acoustic neuroma is a benign growth arising on the eighth cranial nerve. This nerve has two distinct parts, one part associated with transmitting sound and the other sending balance information to the brain from the inner ear. These pathways, along with the facial nerve, lie adjacent to each other as they pass through a bony canal called the internal auditory canal. \n*Acoustic neuromas usually grow slowly over a period of years. They expand in size at their site of origin and when large can displace normal brain tissue. The brain is not invaded by the tumour, but the tumour pushes the brain as it enlarges. The slowly enlarging tumour protrudes from the internal auditory canal into an area behind the temporal bone called the cerebellopontine angle. The tumour now assumes a pear shape with the small end in the internal auditory canal. Larger tumours can press on another nerve in the area (the trigeminal nerve) which is the nerve of facial sensation. Vital functions to sustain life can be threatened when large tumours cause severe pressure on the brainstem and cerebellum part of the brain. \n*Acoustic neuromas large enough to cause hearing loss and other symptoms occur in about one person in 100,000. \n*Most acoustic neuromas are diagnosed in patients between the ages of 30 and 60. \n*The treatment options are observation, surgical removal or radiation

*After Lenneberg (1967) used to be believed that:\n**Aphasia was relatively mild\n**Nearly always recovered completely\n**Non-fluent aphasia is uncommon\n*25-50% have impaired language 1yr post onset (?better outcome with vascular aetiology)\n*Younger age has been linked to greater impairment\n*The full range of adult-like aphasias occur\n*Almost all require extra help at school/special schooling and perform poorly academically\n*Dyslexia and dyscalculia are said to be common

*Most frequently from stroke\n*Or related to sickle cell disease\n*Or traumatic brain injury\n**Commonest cause of death in children after age 2\n

*70% are receiving care in the community\n*30% in residential care

*Aimed at tissue reperfusion to minimise overall damage\n*Control blood pressure to avoid secondary effects\n*Avoid raised ICP\n*[[Clot busting drugs]]\n*[[Reperfusion of the ischaemic penumbra]]\n*[[Carotid endarterecomy]]\n*Therapy to reduce the risk of further stroke\n**Low dose asprin\n*Admission to a specialist stroke unit (higher survival rates, reduced long-term difficulties)\n*Feeding

*Most frequently occur with an acute encephalopathy - due to infection or inflammation\n**Usually [[GTCS|Tonic-clonic seizures (grand mal)]]\n**Require no long-term treatment\n**Benzodiazepam to stop fitting\n**Causes\n***Fluid/electrolyte imbalance\n***Hyper / hypoglycaemic coma\n***Drug withdrawl / poisoning (usually alcohol)

*The majority of epileptic disorders start in childhood - where severe they may persist into adulthood\n**Childhood disorders are nearly all ideopathic - i.e. the primary disorder is the epilepsy\n*When starting in adulthood, they are almost always symptomatic - i.e. a consequence of a neurological disorder, either an [[acute|Acute symptomatic seizures]] effect, or a [[remote|Remote symptomatic seizures]] effect

*Moving too little\n*Examples\n**Drug-induced Parkinsonism\n***Mostly due to neuroleptic (anti-psychotic) drugs\n**[[Parkinson’s disease]]\n**[['Parkinson’s-plus']] \n***[[Wilson’s disease]]\n***[[Multiple systems atrophy]]\n***[[Progressive supranuclear palsy]]\n***Cortico-basal degeneration\n

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*By nasogastric (NG) tube\n*By percutaneous endoscopically-guided gastronomy (PEG) tubes\n*Use of PEG tubes is associated with poorer outcome, but is preferable for long-term feeding - those who cannot swallow safely after 2-3 weeks\n*Delaying the insertion of an NG tube by 7 days does not adversely affect outcome

!Prevalence, etc.\n*The most common cause of dementia - 65% of cases\n*Prevalence - 60-100 per 1000 population of those over 65\n**Prevalence - 300 per 1000 of those over 90\n*Primarily a disease of old age, although early onset AD does occur\n**Early onset AD is often familial\n*[[Risk factors for AD]]\n*[[Treatment for AD]]\n![[Features of Alzeimer's disease]]\n*Gradual onset and progressive decline\n*Impairments are sufficient to cause impairment in ADL\n*[[Definitive (pathological) signs of AD]]\n*[[Brain degeneration in AD]]\n!Language profile in AD\n*[[General language profile in AD]]

*Primarily involves anterior horn cells in the spinal cord and cranial motor nerves\n*Patients may have weakness of bulbar muscles or of single or multiple limb muscle groups. Limb weakness is predominantly distal. Weakness and atrophy of the intrinsic hand muscles are prominent. Weakness progresses to involve the forearms and shoulder girdle muscles and the lower extremities\n*Involvement of both upper and lower motor neurones is characteristic. Patients develop variable hyperreflexia, clonus, spasticity, extensor plantar responses, and limb or tongue fasciculations\n*ALS rarely affects cognitive functions.\n

*[[Anterior circulation]]\n*[[Posterior circulation]]

*Classically involved in reading and writing\n//Dejerine, 1889//

*Supplies\n**Anterior and superior frontal cortex\n**[[Motor cortex (superior)]]\n**[[Prefrontal cortex]]\n**[[Corpus callosum]]

*Large vessels\n**[[Internal carotid artery (ICA)]]\n**[[Middle cerebral artery (MCA)]]\n**[[Anterior cerebral artery (ACA)]]\n*Small vessels\n**Branches of the MCA and the ACA

*Caused by damage to perisylvian regions\n*See [[Aphasia post stroke]] and [[Speech and language disorders after TBI]]

*Rarely (5/18 in Rakowicz and Hodges, 1998)\n*Aphasia is usually non-fluent (3/18)\n*A specific difficulty with verbs has been documented\n*Dementia (2/18)\n**Resembles fronto-temporal dementia\n

!Prevalence\n*Acutely 20-50% of people are aphasic\n*Of these, about 25% will resolve in a few days\n*About 25% of people with stroke will have chronic aphasia\n!Cause\n*Lesions to the dominant hemisphere\n**Right handed people\n***95% are left hemisphere dominant for language\n***Remaining 5% are subject to what is termed //crossed aphasia//\n**Left handed people\n***50% have bilateral language\n***50% have right hemisphere dominant language\n***Recovery from aphasia is often said to be better for left handers\n!Spontaneous recovery\n*Most occurs in the first few months post onset\n*Often said to be complete by 6/9 months post onset\n*Probably continues at an ever decelerating rate for a considerable time post onset\n!Outcome\n*Strongly related to severity\n*Almost all those that are going to recover\n**Will do so in the first few months\n**Have very mild aphasia\n!Variants\n*See [[Neo-classical classification|The Neo-classical Story]]\n*[[Word sound deafness]]\n*[[Right hemisphere language impairments]]\n

*Fibre tract said to join [[Wernicke's area]] and [[Broca's area]]

Inflammation of the arterial wall

Variously associated with lesions to the anterior [[insular cortex|Insular cortex]] //Dronkers, 1996//, and [[Broca's area]] //Hillis, 2003//

*Areas involved in articulation\n**[[Broca's area]]\n**Articulatory motor cortex (must be lesioned bilaterally)\n**[[Supplementary motor area]]\n**Anterior insula - lesions may result in persisting apraxia\n**[[Cerebellum]]\n**[[Brain stem]]\n

*Classically include both\n**Spastic signs\n*and/or\n**[[Cerebellar dysarthria]]\n*In a study, the prevalence of mild to severe dysarthria in an MS population was 51% affecting all components of speech production: respiration, phonation, prosody, articulation and nasality\n*The dysarthria was predominantly mixed, with both ataxic and spastic speech signs frequently present in the speech of a given individual\n*When a predominant type of dysarthria existed, it was not associated with a characteristic profile of neurological deficits\n*Severity of dysarthria was positively correlated to overall severity of neurological involvement, type of disease course, and number of years in progression. \n\n\n\n

*Viral meningitis\n**Viral meningitis most commonly due to [[enteroviruses|Enteroviruses]]\n**And\n***Mumps – but not since MMR\n***Herpes – both simplex and genital\n***And many other viruses\n*Meningitis due to other sources of inflammation\n!Roundup\n*Around 10 per 100,000 pa\n*Less severe than bacterial meningitis\n*Only treatment is ‘conservative’\n*Generally good prognosis

*Caused by a cerebellar lesion – typically as a result of a stroke\n*Results in\n**Intention tremor \n**Difficulty in writing - Dysgraphia with tremor\n**‘Scanning’ dysarthria – reduced intonation, equally stressed, slurred syllables\n**‘Broad based’ gait\n**Clumsiness\n**Incoordination\n**[[Nystagmus]] – inability to perform smooth pursuit in eye movements with saccades substituted\n*Most commonly due to:\n**MS in younger patients\n**Stroke in older patients\n**Toxins: alcohol and some anti-convulsants\n**Also:\n***Tumour, trauma and cerebellar degeneration

*Wide based gait\n*Intention tremor\n*And other symptoms consistent with cerebellar disorder\n*May have cerebellar dysarthria\n*Slurred scanning speech\n*Language and cognitive functions may be relatively normal\n

*Now used almost exclusively with cerebral palsy – writhing movements

*Drop fits\n*Usually in people with significant neurological abnormalities\n*A brief loss of postural tone, often resulting in falls and injuries\n*Ictal EEG similar to that in tonic seizures

*Acute meningitis is almost always bacterial\n*But c75% of people with bacterial meningitis present subacutely\n!Routes for infection\n*From bloodstream\n*From outside – after fracture\n*Direct spread when meninges are breached eg by abscess\n!Due to\n*Haemophilus influenzae – present in 75% of healthy peoples’ nasopharynx\n*Neisseria meningitidis (meningococcus) – often responsible for epidemic meningitis\n*Streptococcus pneumoniae\n*and lots of other rarer causes\n**Now 93% of UK children are immunised against haemophilus and meningococcus C\n!Features\n*Headache\n*Fever\n*Neck stiffness\n*Less frequently\n**Altered consciousness\n**Focal signs\n**Seizures\n!Kernig’s sign\n*Limited by spasm of hamstrings - which in turn causes pain - due to inflammatory exudates around the roots of the lumbar theca\n!In meningococcal meningitis\n*Rash that does not disappear on pressure\n*The glass test\n!Prognosis\n*Affects 5-10 per 100,000 pa; most common in children, but changing with immunisation\n*Without treatment, bacterial meningitis is ~95-100% fatal\n*Mortality was ~50% in mid 1970s\n**Now, with treatment using IV penicillin and cephalosporin,\n*10% mortality in developed counties\n*20% morbidity – most frequently hearing loss, higher function deficits or epilepsy\n

*Large amplitude jerking movements – almost always unilateral so hemiballismus

*Supplies\n**[[Brain stem]]\n***Superior infarcts lead to 'locked in syndrome'\n***Inferior infarcts are often fatal\n**[[Cerebellum]]\n***Infarcts lead to [[Ataxia]], [[Dysarthria]], [[Nystagmus]]\n

*Methods\n**[[CT scans]]\n**[[MRI scans]]\n**[[SPECT]]\n**[[Functional brain imaging]]\n***[[fMRI]]\n***[[PET]]\n**[[EEG and evoked responses (ERPs)]]\n**[[MEG]]\n*[[Brain imaging comparison table]]\n*It is a radiological convention that scans be presented right to left

*There is cell death, resulting in tissue loss - atrophy\n*Causes enlarged ventricles and enlarged sulci\n*Atrophy is particularly prominent hippocampus and the medial temporal lobe\n*This all results in a memory impairment

|!Method|!Radiation dose?|!Magnetic field?|!Expense|!Basic use|!Spatial resolution|!Temporal resolution|!Other comments|\n|CT|Relatively high|No|Cheap|Structural imaging|Good|None||\n|fMRI|None|Yes|Very|Functional imaging - gives whole brain information|Better than PET|1-2 seconds|Noisy, regional lack of sensitivity|\n|PET|High|No|High|Functional imaging - gives whole brain information|2cm|30seconds||\n|ERP|None|None|Cheap|Functional imaging|Not reliable|Milliseconds|Can detect concerted signal from the whole brain|\n|MEG|None|Yes|Expensive|Functional imaging|2 mm|1 ms|Only from regions close to the surface|

*Upper brain stem is essential for conscious control of limbs\n*Lesion results in 'locked in state'

*Due to lesion of [[Broca's area]]\n**Non fluent speech production\n**Impaired repetition\n**Word finding problems\n**Asyntactic\n**Good auditory comprehension

*Damage leads to\n**Articulatory apraxia (at least in the early stages)\n**Expressive and receptive syntactic problems

*A rapidly progressive dementing disease (<6 mos from onset to death)\n*Usually with [[myoclonus|Myoclonus]] (a brief, sudden, singular, shock-like muscle contraction - uncontrolled jerking when attempting to move) \n*Rare \n*Acquired (early onset)\n*New variant (? Related to BSE)\n*Similar to the old fashioned Kuru

*Result in a wide variety of CNS infections including many that are very rare in normal people\n**Toxoplasmosis\n***A focal neurological deficit, headache or seizures developing over a few weeks\n***Prognosis poor\n**Progressive multifocal leucoencephalopathy (PML)\n***Infection with JC virus – a human papilloma virus\n***Progressive deficits affecting occipito-parietal region\n***No treatment\n**Cryptococcal meningitis\n***Presents with headache, malaise and, later, confusion\n***Due to a fungal infection, and treated with antifungals\n**Cytomegalovirus\n***Affects the nervous system at many different levels\n***Can produce an encephalitis, a myelitis or a multifocal neuropathy.\n***Prognosis poor.\n**HIV encephalopathy\n***Initially apathetic\n***Later develops behaviour and memory problems\n***Brisk reflexes and frontal signs\n***May be slowed by antiretroviral drugs

*CT scans use a series of X-ray beams passed through the head. The images are then developed on sensitive film. This method creates cross-sectional images of the brain\n*Shows density of tissue\n*Relatively high exposure to radiation, but no higher than an airline pilot will experience

!NINDS recommended stroke evaluation targets for potential t-PA candidates\n*Door to doctor - within 10 minutes\n*Access to neurologic expertise - within 15 minutes\n*Door to CT scan completion - 25 minutes\n*Door to CT scan interpretation - 45 minutes\n*Door to treatment - 60 minutes\n*Admission to monitored bed - 3 hours\n!What happens in the UK at the moment\n*22% of stroke patients have a scan on day of onset\n*Those patients who were registered as requiring an urgent CT scan, only 30% actually got the scan on the same day\n*Current thrombolysis rates <1%\n*If increased to 9% (as has been acheived in some parts of the US and Australia), would save £16 per annum

*Surgical procedure\n*Removal of [[clot in carotid artery|Clots in the Carotid Artery]]\n*Done using a balloon scouring backwards\n*Can be done post stroke as a preventative measure\n*Reduces risk of second stroke within three years by 50%

*A defect in the transmission of nerve impulses to muscles – in the neuromuscular junction\n*Antibodies produced by the body's own immune system block, alter, or destroy the receptors for acetylcholine\n*So it is an autoimmune disease\n

*Probably due to inappropriate activation of glutamate receptors \n

*Largely unknown\n!Prevalence of MS increases as you get further from the equator\n*Sussex - 111 per 100,000\n*Orkney - 258 per 100,000\n*This has led to a range of suggestions as to why\n**Exposure to viral or bacterial infections\n**Environmental toxins\n**Duration of sunlight\n**Temperature or humidity\n**Diet \n!Infection\n*Some viruses can cause demyelination in the brain and spinal cord of humans and animals\n*MS attacks are more likely during non-specific viral syndromes than they are at other times. But, the clinical pattern of disease following such infections is not identical to MS\n*Viral proteins have not been reliably isolated from MS brains\n*The relationship between MS and infectious agents (e.g., human herpes virus-6, chlamydia, etc.) remains uncertain\n!Genetic\nGenetic\n*2x risk in women cf men\n*MS is common in Caucasians but occurs rarely in Native Americans, Blacks native to Africa, and Asians living in high-risk areas in the United States \n**This suggests that if an environmental factor contributes to MS, only those who are genetically susceptible actually develop the illness\n*Risk in (US) population is c0.15% but 1-4% for those with 1st degree relative affected\n*Risk for a dizygotic twin is approx 2% but for a monozygotic twin is 25-30%\n**So a substantial genetic influence\n**But also a strong environmental influence because only a minority of genetically identical twins are both affected with MS\n!Infection\n*May begin with an infection by a virus or other external antigen \n*It is "eaten" by a macrophage, which digests the proteins of the virus or antigen to form peptides\n*White blood cells bind to the myelin system in the brain\n\n

*RTA\n**~RTAs are the commonest cause of death 10-65\n**Motorcyclists are at particular risk\n*Assaults (and war)\n*Falls (especially in the elderly, people with [[Epilepsy]])\n*Sports injuries

*Infarcts lead to Ataxia, Dysarthria, Nystagmus\n*Needed for accurate motor control\n*Alcohol is toxic to the cerebellum

*Skull\n*Dura\n*Arachnoid\n*Pia Mater\n*Brain

*Now rare\n*From:\n**Direct spread into brain from adjacent tissues (75%), eg sinus infection, middle ear\n**Via blood (25%) from other source of infection\n*Present with:\n**Progressive headache 75%\n**Focal signs 50%\n**Fever 50%\n**Seizures 30%\n*In immunocompromised people\n**People are usually immunocompromised by\n***Iatrogenic reasons eg chemotherapy or after transplant surgery\n***Severe general illness eg diabetes or lymphoma\n***A specific immunodificiency eg [[AIDS|CNS infections in HIV and AIDS]]\n*The first two\n**Result in a variety of bacterial and fungal infections of the CNS\n**Difficult to diagnose because so atypical

!What is CP?\n*a developmental disability that results from damage to or dysfunction of the developing brain. \n*non-progressive but permanent. \n*varying degrees of disability related to:\n**functional mobility (movement and posture), \n**daily living skills\n**communication / socialisation skills\n!Incidence\n*Cerebral palsy is the most common physical disability in childhood.\n*The frequency of cerebral palsy has not changed over the past 40 years.\n*Decline followed by increase \n*Incidence around 2 per 1000 live births\n*More frequent in low birth weight babies\n*75% due to congenital or prenatal factors\n*15-20% due to perinatal factors\n!Classification in terms of pattern of motor disability\n*[[Spastic hemiplegia]] c30%\n*[[Spastic diplegia]] c40%\n*[[Spastic quadiplegia]] c8%\n*[[Dyskinetic CP]] c10%\n*[[Ataxic CP]] c12%\n

*[[Developmental disorders]]\n**[[Congenital disorders]]\n***[[Hereditary disorders]] (many of these may not become apparent until later)\n****[[Fragile X syndrome]]\n****[[Williams syndrome]]\n****[[Down's syndrome]]\n****[[Friedreich's ataxia]]\n***Disorders acquired in utero in the course of development\n****[[Congenital rubella]]\n****[[Spina bifida]]\n****[[Cerebral palsy]]\n***Disorders acquired perinatally\n****[[Cerebral palsy]]\n****[[Very low birthweight children]]\n***[[Acquired lesions and disorders|Acquired lesions and disorders (childhood)]]\n****[[Perinatal stroke]]\n****[[Sickle cell disease]]\n****[[Acquired aphasia in children]]\n****[[Landau-Kleffner Syndrome]]\n***[[Other acquired neurological disorders in childhood]]

*They look like a [[GTCS|Tonic-clonic seizures (grand mal)]]\n*The most common seizure disorder in childhood\n*Usually occurring with high fever\n*Occur in 2-5% of children aged 6 months to 5 years\n*Usually only occurs once (66% of the time)\n*Related risk of a seizure disorder by age 25 is 2.5% - doubling the risk

*Jerky, restless, purposeless movements giving a fidgety appearance\n*There are a variety of very unusual causes of chorea\n**Sydenham’s chorea\n**Senile chorea\n**Vascular chorea\n**And of course [[Huntingdon's disease]]

*Physiotherapy\n*OT\n*SLT\n*Return to work\n*Return to the community

*Gait\n**Considerations\n***Symmetrical?\n***Posture: stooped or erect?\n***Step size: normal or shortened?\n***Knee lift: normal or high stepping?\n***Arm swing: normal or reduced?\n**Clinical signs\n***Broad-based gait with unsteadiness suggests cerebellar [[ataxia|Ataxia]]\n***Small steps with increasing frequency – a festinating gait - suggests [[Parkinsonism]]\n***Asymmetry suggests spasticity/stroke\n*Heel-toe walking:\n**A sensitive test for [[ataxia|Ataxia]]\n*Romberg test:\n**Stand feet close together, then close eyes\n**If they fall with eyes closed Romberg test is failed\n*Finger-nose coordination\n*Repeated movements\n**For example\n***Back and front of hand\n***Finger-thumb\n***Tapping\n***Wrist pronation and supination\n**Clinical signs\n***Upper motor neurone – pyramidal – lesions result in slow and deliberate movements\n***In extrapyramidal disorders, movements start slowly, becoming progressively smaller in amplitude\n*[[Tremor]]

*The [[tonic stage|Tonic phase: tonus]] gives way to clonic convulsive movements, in which the tonic muscles relax intermittently, lasting for a variable period of time\n*During this stage, a generalised tremor occurs at a rate of 8 tremors per second, which may slow to about 4 tremors per second\n**This is because phases of atonia alternate with repeated violent flexor spasms.\n***Each spasm is accompanied by pupillary contraction and dilation\n*The atonic periods gradually become longer until the last spasm\n*Voiding may occur at the end of the clonic phase as the sphincter muscles relax\n*The atonic period lasts about 30 seconds - with the patient remaining apnoeic\n*The convulsion, including tonic and clonic phases, lasts for 1-2 minutes

*Rhythmic, motor, jerking movements with impairment of consciousness\n*Could have a focal origin with or without impairment of consciousness\n**The focal seizures are classified as simple or complex partial seizures\n*Typically, generalised clonic seizures simultaneously involve the arms and legs\n*Ictal EEG shows bilateral rhythmic epileptiform discharges

*Also known as Thrombolytics, Recombinant tissue plasminogen activator - t-PA\n*Must be given within three hours of onset\n*Patients treated with t-PA are 30% more likely to have minimal or no disability at 3 months post onset\n*Mortality at 3 months post onset reduced from 21% to 17%\n*Side effect - increased risk of intracerebral [[haemorrhage|Haemorrhage]]\n!Criteria for getting t-PA\n*Ischaemic stroke in [[last 3 hours|Care Pathway In Stroke]]\n*CT [[scan|Care Pathway In Stroke]] with no evidence of haemorrhage\n*No stroke or TBI within last 3 months\n*No history of brain haemorrhage\n*No history of gut or urinary tract haemorrhage\n*No significant hypertension\n*Not taking anticoagulants

The most common cause of [[embolic stroke|Embolic Stroke]]

*Result in surprisingly mild deficits perhaps because the allow for relocalisation of function\n*The effects depend on the localisation of the tumour\n

*Consciousness is impaired - unable to remember the event\n*Often can remember aura\n*Typically, begins with behavioural arrest, followed by staring, automatisms, and postictal confusion\n**Typically lasts for about 60-90 seconds\n*Generalised weakness or fatigue may last for a few days\n*CPS of medial temporal lobe origin\n**Dystonic posturing of the contralateral arm\n*CPS of frontal lobe origin\n**May feature bizarre motor behaviours such as bicycling or fencing posture\n*Generally has an ictal correlate in the EEG

*[[Posttraumatic epilepsy]]\n*[[Posttraumatic headaches]]\n*[[Posttraumatic movement disorders]]\n*[[Posttraumatic psychiatric disorders]]\n*[[Speech and language disorders after TBI]]

*Due to lesion of the [[Arcuate fasciculus]]\n*Fluent paraphasic speech production\n*Impaired repetition\n*Good auditory comprehension

*Hereditary (many of these may not become apparent until later)\n*Acquired in utero in the course of development\n*Acquired perinatally\n

*German measles in a mother in the first trimester of pregnancy is very likely (c85%) to result in congenital rubella syndrome\n*During 1964 and 1965 a rubella epidemic in the United States caused an estimated 12.5 million cases of rubella and 20000 cases of congenital rubella\n*Now very rare because of immunisation\n*Can affect virtually all organ systems. \n*Deafness is the most common and often the only symptom of congenital rubella infection (especially after 1st trimester)\n*Eye defects, including cataracts, glaucoma, retinopathy, and microphthalmia may occur\n*Cardiac defects such as patent ductus arteriosus, ventricular septal defect, etc are common. \n*Neurological abnormalities, including microcephaly and learning disability often occur\n*Created a large population of the ‘deaf-blind’

*Intracranial haemorrhagic lesions in 27% of patients\n*Traumatic [[subarachnoid haemorrhage|Subarachnoid Haemorrhage]] in 39% of patients\n*Diffuse cerebral [[oedema|Oedema]] was present in 39% of patients

*Responsible for communication between the hemispheres

*Susceptible to\n|!Coup|!Contracoup|\n|Frontal|Occipital|\n|Front end of temporal lobe||

|!Nerve|!Motor|!Sensory|\n|V Trigeminal|Muscles of mastication|Tongue, face, mouth|\n|VII Facial|Lip closure|Taste|\n|X Vagus|Palate, larynx, pharynx|Larynx, pharynx|\n|XII Hypoglossal|Tongue||

*Around 50% of people with DLB go on to develop a Parkinsonian movement disorder\n*Around 25% of people with Parkinson’s disease go on to develop DLB\n*Both DLB & Parkinson’s disease are characterised by Lewy body inclusions\n*But mostly cortical in DLB\n*And predominantly sub-cortical (esp. in substantia nigra) in PD\n

*Progressive muscular weakness\n*Average survival from the start of symptoms is only about three years\n**Longer in younger patients\n*Causes progressive injury and cell death of lower motor neurone groups in the spinal cord and brain stem and usually also of upper motor neurones in the motor cortex. \n*Those affected typically develop a combination of upper and lower motor neurone signs\n**progressive muscle weakness and wasting \n**usually pathologically brisk reflexes, eventually involving the limb and bulbar muscles. \n*Death usually results from respiratory failure due to weakness of the ventilatory muscles

[[Welcome]]

*Neurofibrillary tangles and amyloid (senile) plaques

|!Dementia|!Frequency|!Prevalence|!Memory disturbance|!Accompanied by|!Language features|!Onset|!Decline|\n|[[Alzheimer's disease]]|50-65% of dementias|60 per 1000 over 65s|Primarily episodic, and semantic|At least one of aphasia, apraxia, agnosia, executive impairment|Anomia, empty, fluent speech|Gradual|Progressive|\n|[[Vascular dementia]]|10-50% of dementias|30 per 1000 over 65s||Gait disturbance, executive functioning, psychomotor slowing|Dysarthria, dysphasia, aphasia|Abrupt|Stepwise|\n|[[Demetia with Lewy Bodies]]|||Episodic memory often relatively well-preserved initially, Semantic memory impairment|Progressive cognitive decline, with two of: Fluctuations in consciousness, Visual hallucinations, Parkinsonian motor features, also executive disorder|Anomia, topic shifts, fluctuations||\n|[[Fronto-temporal dementia - Temporal variant]]|||Episodic memory relatively good||Semantic deficit, empty fluent speech||\n|[[Fronto-temporal dementia - Frontal variant]]|||Episodic memory relatively good|Executive disorder|||\n|[[Progressive non-fluent aphasia]]|||Episodic memory relatively good|Executive disorder|Phonological / syntactic difficulties||

*Progressive cognitive decline, characterised by (at least two of)\n**Fluctuations in consciousness\n**Recurrent visual hallucinations\n**[[Parkinsonian|Parkinsonism]] motor features (rigidity; bradykinesia; rest tremor)\n*Frequent features: deficits in:\n**Perceptual and visuo-spatial skills \n***Drawing poor\n***Easily gets lost\n***Visual hallucinations\n**Attention\n**[[Executive functions|Frontal damage]]\n***Poor performance on Stroop test\n****What colour does it say, when it's written in a different colout\n***Poor performance on Wisconsin card sorting (according to shape - switching of criteria for sorting)\n**[[Episodic memory|Episodic memory impairment]] often relatively well-preserved, at least in the early stages\n***Visual memory typically worse than verbal\n***[[Semantic memory impairment]] is similar to AD\n*[[Treatment of DLB]]\n*[[DLB and Parkinson's disease]]\n*[[Language profile in DLB]]\n*[[Distribution of pathology in DLB]]\n

*[[Frontal lobe syndrome|Frontal damage]]\n*Memory disorders\n**Both retrograde and anterograde amnesia\n*Visual disorders\n**Due to damage to the occipital pole - primary visual cortex\n**Also due to damage to the optic nerves that run across the base of the brain

*Developmental disorders often impact\n**Development of language\n**Development of other cognitive skills\n**Behaviour – directly or indirectly\n**Typically affect multiple organ systems\n**Nervous system\n**Heart\n**Liver, kidneys …\n

*The diagnosis of clinically definite MS requires:\n**Two distinct episodes of symptoms and two or more signs evident on the neurological examination\n**Episodes of symptoms must last at least 24 hours and be separated by one or more months\n*Signs must be due to involvement of 2 or more separate parts of the brain and spinal cord

*Areas may not function properly because they are deprived of some of their usual inputs by a lesion\n*This would lead to an observed depression in the local metabolism\n*These remote effects may be temporary\n//Monakow (1914)//

*Temporal lobe relatively unaffected\n*Occipital, frontal and parietal lobes

*Trisomy of chromosome 21\n!Incidence\n*1 in 1,250 for birth to a mother at age 25\n*1 in 100 for birth to a mother at age 40. \n*Most babies with Down syndrome are born to women under age 35 because more younger women have babies.\n!Effects\n*Very variable \n*Most people with Down syndrome have IQs that fall in the mild to moderate range of mental retardation\n*may have delayed language development and slow motor development. \n*Some common physical signs of Down syndrome include:\n**Flat face with an upward slant to the eye, short neck, and abnormally shaped ears\n**Deep crease in the palm of the hand\n**Poor muscle tone, loose ligaments\n!Associated health conditions\n*Congenital heart disease\n*Hearing problems\n!Outcome\n*Life expectancy increased from 25 to 49 from 1983 to 1997 in the USA\n*A raised incidence of Alzheimer’s disease in these elderly\n*And increased rates of dysphagia

*Caused by weakness\n*Depends on the muscle groups most involved\n*Hypophonia (weak voice)\n*Hypernasality\n*Slurred articulation\n

*Hypophonic\n*Hypotonic: weak, slurred articulation\n*Hypernasality\n*Breathiness/hoarseness\n*Due to weakness and paralysis of the lips, facial muscles, tongue, larynx and pharynx resulting from affected trigeminal, facial, glossopharyngeal, vagus, accessory

*Moving too much\n*Diagnosis\n**Rhythmic, sinusoidal movements: [[tremor|Tremor]]\n**[[Jerks]]\n**Muscle spasms, twisting, sometimes repetitive: [[dystonia|Dystonia]]\n**Writhing movements: [[athetosis|Athetosis]]\n

*Involves basal ganglia and/or extrapyramidal pathways\n*Athetoid (writhing) movements or dystonia\n*Dysphagia and dysarthria are very common\n*Language and cognitive skills usually relatively normal\n

*Can result in\n**Aspiration - resulting in severe risk of pneumonia\n**Malnutrition - resulting in greater mortality and morbidity\n**Is associated with much higher mortality, but partly because of brain stem stroke\n*Control of swallowing\n**[[Cranial nerves involved in swallowing]]\n**[[The central pattern generator]]\n*[[Alternative feeding]]\n*[[Predictors of outcome]]

*Caused by weakness\n*Depends on the muscle groups most involved\n*Jaw weakness affects chewing esp. late in the day\n*Tongue, palate and pharynx weakness exacerbate the problem\n*Weakness of head extensors can exacerbate difficulties\n

*Sustained muscle contractions, frequently causing twisting and repetitive movements and abnormal postures

*EEG\n**In EEG, a number of electrodes are placed over the scalp and record the activity of neurons over a period of time. \n**The EEG trace varies according to the general state of the brain: when the subject is quiet or asleep, EEG is synchronised, which means that it has a wave-like shape, with waves being of a particular amplitude and frequency (usually alpha waves, 8-12 Hz). \n**When the subject is awake and active, EEG is desynchronised, which means there is no repetitive wave pattern, but an irregular electrical activity\n*~ERPs- event-related potentials\n**Consist of a sequence of positive and negative voltage deflections (components) that have characteristic time delays and wave shapes.\n**The evoked response to a single stimulus at the scalp is quite small and is extracted from the background activity by averaging. Averaging enhances the signal and reduces the noise to nearly zero. \n**Brain activity is revealed by ERPs with a high degree of temporal precision (of the order of milliseconds), \n**But with poor-to-non-existent spatial resolution

*Deal with the [[haemorrhage|Haemorrhage]]\n*Prevent the rise in ICP\n*Maintain good cerebral perfusion through preventing hypotension\n*If closed HI with no loss of consciousness- discharged if x-rays and brain signals are normal\n*If history of loss of consciousness\n**There is an increased risk of hairline fractures of the base of skull\n**This can lead to sudden [[haemorrhage|Haemorrhage]]\n**Usually admitted for 2-hourly observations

!General\n*Depends on the areas of cortex lost\n*Lesions typically result in both:\n**A cortical lesion (grey matter)\n**Disconnection of areas connected by white-matter tracts, both cortical-cortical tracts, and cortical-subcortical tracts\n!Variability of effects\n*Small differences in site of lesion can mean a difference of vast numbers of differently affected fibres\n*Different people locate functions differently in the cortex\n*Variable effects of lesions to distant areas - [[diaschisis|Diaschisis]]\n*Variable areas not functioning - the ischaemic penumbra\n**These cells may look well, but they may not be getting enough blood to function properly\n*Variable amounts of recovery / take over of function by other areas - e.g. in undamaged ipsilateral areas or homologuous contralateral areas\n*Areas supplied by different cerebral arteries vary radically\n!So\n*The relationship between lesions and symptoms is not 1:1

*Complete or partial occlusion of arteries\n*Part of a blood clot elsewhere breaks off and then lodges in an artery - blocking it\n*Can come from thrombus formed for any reason\n**Ulcerated arterial lesion - most common, especially in the [[carotid artery|Clots in the Carotid Artery]], sometime vertebral\n**[[Mitral valve]] disease\n**[[Myocardial infarction]] having damaged left side of the heart\n***Leading to mural thrombi, left atrial thrombus, etc

*Infection of the brain\n*Incidence 5-15 per 100,000 pa\n*Mostly viral. Most commonly due to:\n**[[Herpes simplex virus (HSV)|Encephalitis secondary to HSV]]\n**[[Measles|Encephalitis secondary to Measles]]\n**Mumps\n**Rabies\n**Arboviruses (from ticks, mosquitoes etc)\n!Course of encephalitis\n*Illness with fever, malaise, myalgia\n*Headache, fever, neck, stiffness (due to meningism)\n*Mental change, disorientation, dysarthria, aphasia, drowsiness/coma\n*Focal signs: hemiparesis, sensory loss, spasticity \n*Oedema, raised intracranial pressure\n!Enters brain either:\n*From blood stream\n*Or centripetally up nerves: ‘retrograde neural dissemination’ \n*Is a very rare complication of systemic viral infection

*Herpes simplex encephalitis\n*HSV is very common; responsible for cold sores\n*Probably transmitted up the trigeminal nerve to the brain\n*c10% of viral encephalitis\n*Treated with acyclovir\n*Reduces mortality from c70% to around 30% if given early\n!Presentation\n*Worst affects are on temporal lobe, particularly inferior and medial regions\n*Results in memory impairments – anterograde and retrograde amnesia from hippocampal and parahippocampal damage\n*Results in semantic deficits from inferolateral temporal damage\n!~Kluver-Bucy Syndrome\n*In the acute stages “~Kluver-Bucy Syndrome” is common\n*Due to bilateral destruction of the amygdala and inferior temporal cortex \n*Emotional blunting: flat affect and may not respond appropriately to stimuli. \n*Hyperphagia: compulsively place inedible objects in their mouths \n*Inappropriate sexual behaviour: may fail to publicly observe social sexual norms and there may be an increase in their sexual activity\n*Visual agnosia: Oral compulsions may provide an alternate means of object identification\n!Long term effects\n*The following are frequent:\n**Amnesia\n**Semantic impairments\n***Sometimes, but not necessarily, affecting animate items particularly\n**Emotional changes

Measles\n*0.2 to 1 cases of encephalitis per 1000 cases of measles\n*More frequent as get older\n*Severe encephalitis\n*15% mortality\n*50-90% have severe neurological sequelae\n*SSPE – subacute sclerosing panencephalitis\n**Occurs in 5-9 cases per million following measles (1/10th rate following immunisation)\n**Severe, rapidly developing brain degeneration resulting in death in 96% of children within two years\n

*Enteroviruses are a large family of viruses responsible for many infections in children. These viruses live in the intestinal tract, but can cause a wide variety of illnesses. There are more than 70 different strains, which include the group A and group B coxsackieviruses, the echoviruses, the polioviruses, Hepatitis A virus, and several strains that just go by the name enterovirus. Even though there are many strains, most illness is caused by about a dozen of them. Most children develop immunity to them and don’t get a strain more than once.

*Neurones in a focus are hyperexcitable and, for unknown reasons, remain in a state of partial depolarisation\n*The neurones surrounding the focus inhibit the epileptogenic neurones

*Affects visual and verbal memory\n*Graded retrograde amnesia\n*Anterograde amnesia\n*Due, probably, to hippocampal and medial and temporal tissue loss (including the parahippocampal gyri)

*Composed of\n**Basal ganglia:\n***Thalamus (ventrolateral nucleus)\n***Caudate\n***Putamen\n***Globus pallidus\n***Substantia nigra\n***Subthalamic nucleus\n**Cerebellum\n***And pons\n*It is an extremely rich and complex system\n*The cerebellum has as many cells as the cerebral cortex\n*The cerebello-pontine system contains 20x as many cells as the pyramidal tracts\n*It is responsible for\n**The co-ordination of movement\n**Integration of movement with proprioceptive inputs\n**Modulation of movement\n**Control of movement\n*It is not conscious\n*Disorders result in\n**Incoordination of movements\n**Difficulties in initiating, sustaining or terminating movements\n**Poor integration of movement control with sensory inputs\n**But relatively normal power and extent of movement

*Extrinsic – arise from intracranial structures outside the brain\n*Meningioma 15%\n**Arise from arachnoid cells \n**May erode bone\n*Pituitary adenoma 7%\n**Chiasmatic visual disturbances and endocrine effects\n*Schwannoma 7%\n**Eg of acoustic nerve - benign\n

*More favourable if:\n**Female\n**onset earlier than 40 years\n**first attack optic neuritis or other sensory symptoms\n**lack of significant disability 5 years after onset, \n**minor abnormalities of brain MRI scan at the time of diagnosis. \n*Less favourable if:\n**difficulty walking or sustained impairment in coordination after first attack has resolved\n**large number of MRI lesions seen at first diagnosis\n

*Poorer outcome\n**Lower [[GCS]] scores\n**Longer period of unconsciousness\n**Increasing severity of injury

!Memory disturbance\n**First presenting symptom often [[episodic memory disturbance|Episodic memory impairment]]\n***Anterograde and retrograde amnesia (could be because these memories were laid prior to diagnosis)\n***Early memories are relatively well-preserved\n**[[Semantic memory impairment]]\n**STM is comparatively good\n!Memory impairment is accompanied by one or more of\n**[[Aphasia]]\n**[[Apraxia]]\n**[[Agnosia]]\n**[[Executive impairment|Frontal damage]]\n!Atypical presentations\n*Where the first feature is usually primarily\n*[[Apraxia]] (?parietal)\n*[[Executive impairment|Frontal damage]] (?frontal)\n*Visuo-spatial problems (?occipito-parietal)\n \n

*Early features typically include:\n**Gait disturbance, unsteadiness and falls\n**Personality, mood and executive impairments\n**Psychomotor slowing

!Incidence\n*the most common inherited cause of learning disability\n*Incidence 25 per 100,000 \n*Due to an X chromosome defect\n*So males more likely to be severely affected\n!Physical characteristics\n*In boys:\n**elongated face, large head, and prominent ears \n*In girls:\n**Relatively normal\n!Cognitive/behavioural characteristics\n*Most males and 1/3 females significant intellectual impairment\n*Poor social skills\n*Poor eye contact \n*social avoidance\n*Stereotypic/repetitive behaviours\n*Hyperactivity\n*7-25 % autistic\n*Great phenotype variability \n!Language profile\n*Delayed, but typically in line with intellectual abilities\n*Some evidence production more affected than comprehension\n*Many esp those with autism are almost completely non-verbal \n*Persistent phonological/articulatory difficulties\n*Harsh voice\n*Rapid & variable speech

*Around 300,000 head injuries in the UK each year\n**75% mild\n**Around 15,000 deaths per annum\n**313 hospitalisation per 100,000\n*Numbers have fallen following widespread use of seatbelts and helmets\n*65% are men\n*Half of head injury hospitalisations are for people under 24

*Autosomal recessive inherited disorder\n*Affects 1 in 50,000\n*Age of onset typically 5-15\n*Progressive degeneration caused by demyelination of nerves in the spinal cord, cerebellum and lower motor neurones\n*Typically wheelchair bound after 10-20 years\n*First symptom usually gait ataxia. The ataxia gradually worsens and spreads to the arms and then the trunk \n*Dysarthria (slowness and slurring of speech) develops (and may be the first symptom)\n*Slowed syllables and difficulty with repetitive oral/speech movements prominent (Ziegler, 1996)

*Prefrontal lobes\n**Needed for executive functions\n***Initiating actions\n***Terminating actions\n***Judging appropriateness of actions\n***Deciding which actions to perform\n*Other frontal signs\n**Changes in personality\n**Emotional lability\n**Emotionally inappropriate responses\n*Symptoms of executive disorders\n**Apathy\n**Silence\n**Failure to initiate actions\n**Performance good in elicited actions\n**Failure to terminate actions\n***Perseveration\n***Difficulty with task switching\n*Related to a failure of judging appropriateness of actions\n**Sexual remarks / groping\n**Inappropriately humorous behaviour\n**Inappropriate rudeness\n**Aggressive behavious\n*Related to deciding which actions to perform \n**Difficulty with carrying out several tasks simultaneously\n**Impulsiveness\n**Inappropriate stimulus-led behaviour 'perplexia'

*Due to brain atrophy primarily affecting the inferolateral frontal cortex and the lateral temporal lobe\n*Medial temporal lobe is relatively well-preserved\n*As a result episodic memory is relatively good – often wholly normal in the early stages\n*Most prominent impairments:\n*Executive, personality change, moods (from frontal deficit)\n*Semantic deficit (from temporal lesions)\n

*See [[Frontal temporal dementias]]\n*Due to brain atrophy primarily affecting the inferolateral frontal cortex \n*Medial temporal lobe is relatively well-preserved\n*As a result episodic memory is relatively good – often wholly normal in the early stages\n*Most prominent impairments:\n**Executive, personality change, moods\n***Psychiatric abnormalities that seem to respect the pattern of the classic frontal lobe syndromes are present\n****Patients with orbitofrontal dysfunction become aggressive and socially inappropriate. They may steal or demonstrate obsessive or repetitive stereotyped behaviours\n****Patients with dorsomedial or dorsolateral frontal dysfunction may demonstrate a lack of concern, apathy, or decreased spontaneity\n****Patients may be depressed early in the disease\n***These mood changes can predate amnesia\n**Speech and language abnormalities often begin early and progress rapidly\n**Memory impairment is relatively less severe than speech/language and behavioural changes\n*Pathology unclear (may be [[Pick's disease]])

*See [[Frontal temporal dementias]]\n*Due to brain atrophy primarily affecting the lateral temporal lobe\n*Medial temporal lobe is relatively well-preserved\n*As a result episodic memory is relatively good – often wholly normal in the early stages\n*Most prominent impairments:\n**Semantic deficit \n*[[Language profile in Fronto-temporal dementia - Temporal variant]]\n*Often continue to operate premorbid skills to a very high level\n*In the long term progresses to a global dementia\n

*both techniques can be used to examine the distributions of particular chemicals.\n*The most common method is to detect ~rCBF – regional cerebral blood flow.\n*PET does this by using O15 labelled ~CO2\n*Both ~fMRI and PET\n**Go through complex signal processing and statistical analysis\n**Resulting in effects mapped in 3 dimensions\n**Changes are much more substantial in cortex – grey matter – than sub-cortical changes\n**Measure rCBF changes so temporal resolution can never be better than c 2secs\n**But spatial resolution is good\n

*Eyes open\n|Spontaneously|4|\n|To verbal stimuli|3|\n|To pain|2|\n|Never|1|\n*Best verbal response\n|Orientated and converses|5|\n|Disorientated and converses|4|\n|Inappropriate words|3|\n|Incomprehensible words|2|\n|No response|1|\n*Best motor response\n|Obeys commands|6|\n|Localises pain|5|\n|Flexion withdrawl to pain|4|\n|Abnormal flexion (decorticate rigidity)|3|\n|Abnormal flexion (decerebrate rigidity)|2|\n|No response|1|\n\n*Total GCS scores\n|Mild head injury (concussion)|13-15|\n|Moderate head injury|9-12|\n|Severe head injury|3-6|\n

*Naming impairment\n*Syntax and phonology relatively well preserved\n*Good repetition, and reading of regular words\n*Empty fluent speech\n*Pragmatically odd – forgetting topic of conversation\n

*May start in adulthood\n**[[Tonic-clonic seizures (grand mal)]]\n**[[Myoclonic seizures]]\n**[[Absences (petit mal)]]\n*Always start in childhood\n**[[Tonic seizures]]\n**[[Atonic seizures]]\n**[[Clonic seizures]]\n*[[Seizure mechanism]]

*A ‘common’ disease\n*Prevalence c50 /100,000\n**Approx 4x as common in men\n*Onset early – mean age 7yrs\n*Vocal tics – sniffs, coughs and grunts are common\n*Coprolalia – swearing – is much rarer and develops later\n

*Due to lesion of both [[Broca's area]] and [[Wernicke's area]]\n*Very impaired speech production\n*Impaired repetition\n*Impaired auditory comprehension

*Intracerebral\n**Bleeding into the brain itself\n*[[Subarachnoid|Subarachnoid Haemorrhage]]\n**Bleeding into the [[subarachnoid space|Subarachnoid Space]]\n*Subdural\n**Bleeding into the [[subdural space|Subdural Space]]

*[[What is head injury (HI) or Traumatic brain injury (TBI)]]\n**[[Frequency of TBI]]\n**[[Causes of TBI]]\n**[[Risk factors for TBI]]\n**[[Factors affecting outcome in TBI]]\n*[[Consequences of TBI]]\n**[[Neurochemical consequences of TBI]]\n**[[Physiological consequences of TBI]]\n**[[Unconsciousness after TBI]]\n***[[Glasgow Coma Scale|GCS]]\n***[[Post traumatic amnesia (PTA)]]\n****[[Mini-mental state examination]]\n*[[Early management in TBI]]\n*[[Prognosis]]\n*[[Complications]]\n*[[Descriptions of common types of brain damage]]

**Show considerable phenotype variability\n**Can now show who has the genes and clear that the degree to which they are expressed can vary\n

*The primary auditory cortex\n*Damage here leads to cortical deafness (with bilateral lesions)

*Due to a dominant gene\n*50% of people with a parent with HD will develop the disease\n*Mostly developed between 30 and 60\n*Prevalence varies\n**6 per 100,000 in US\n**0.1 in Japan\n**0.5 in Finland\n**7.8 in Malta\n**700 around Lake Maracaibo in Venezuela\n*Symptoms\n**Chorea\n***Especially in face and upper limbs\n**[[Dysarthria]]\n**Psychiatric disorders\n***Irritable, difficult, suicide\n**Cognitive impairment (dementia)\n***Poor at memory & arithmetic with executive disorders\n

!Incidence\n*1-2 per 1000 people per annum\n*Approximately 100,000 new or 'recurrent' strokes in the UK each year\n*Around half will die from stroke\n!Prevalence\n*Around 300,000 people in the UK are stroke survivors\n!Ranking\n*Third most frequent cause of death behind heart disease and cancer\n*The most frequent cause of long-term disability\n*The most expensive disorder to society

*About 3.5% of people are diagnosed as having seizures at some point in their lives\n*About 9% of people actually have seizures at some point in their lives\n*Prevalence of [[active epilepsy|Active epilepsy in the UK]] is around 4-10 per 1000\n*Incidence (first seizures) is between 25-50 per 100,000 between 10 and 70\n*Much higher in children, declining from 150 to 40 per 100,000 between 0 and 10\n*Rising again after age 65 to around 100 per 100,000 at 75\n*Rate of [[sudden death|SUDEP]] is about 24 times higher in people with epilepsy\n*In uncontrolled epilepsy, elevated risk of head injury from repeated falls, and risk of cerebral atrophy from repeated anoxic episodes during seizures

*In adults primary intracranial tumours represent only 3% of tumour deaths and 1% of all deaths\n*Incidence is 4-7 per 100,000\n*Intracranial metastases (secondaries) are more common.

*Three types:\n**[[Embolic Stroke]] \n**[[Thrombotic Stroke]]\n**[[Small Vessel Disease or Lacunar Stroke]]\n\n*Complete or [[partial|Note1]] occlusion of arteries\n*When blood flow drops\n**Cells die from lack of oxygen and build up of [[toxic wastes|Toxic Waste In Infarction]]\n**Necrosis\n*Infarcted area is surrounded by an [[ischaemic penumbra]]\n**Regions where blood flow is reduced, and cell death will follow in hours or days\n**At least partly due to arterial spasm

*[[Infections are rare]]\n*Types of infection\n**[[Meningitis]]\n***[[Bacterial meningitis]]\n***[[Aseptic meningitis]]\n***[[Tuberculous meningitis]]\n**[[Encephalitis]]\n**Other infections of the CNS\n***[[Neurosyphilis]]\n***[[Cerebral abscess]]\n***[[CNS infections in HIV and AIDS]]

*Because the CNS is protected by blood brain barrier (cerebral endothelial cells and the basement membrane surround blood vessels so that large molecules and cells cannot enter the brain), infections are relatively rare in developed countries\n*Much more common for people in ‘immunocompromised states’ (inc AIDs)\n*And in poverty\n

*Incorporates\n**[[Supramarginal gyrus]]\n**[[Angular gyrus]]\n*Located\n**Immediately above [[Wernicke's area]]

*Incorporates\n**[[Broca's area]] (in dominant hemisphere)\n**Articulatory motor cortex\n***There is bilateral innervation to muscles of articulation\n***Therefore there needs to be a bilateral lesion for a cortical dysarthria\n**Face and arm motor and sensory cortex\n***Leads to contralateral facial palsy with sensory loss\n***Spastic arm (because it is the //upper// motor neurone) - an upper limb hemiparesis with sensory loss

*Damage leads to\n**[[Articulatory apraxia]] (in the anterior insular cortex, //Dronkers, 1996//\n**Other functions unclear - possible developmental dyslexia\n*Location\n**Not visible - it is inside the Sylvian fissure

*Intrinsic – arising within the substance of the brain\n*Glioblastoma 20%\n**Glial cells – poor prognosis\n*Astrocytoma 10%\n**Astrocytes – relatively benign - c70 mo survival\n*Metasteses 10%\n**Poor prognosis\n*Oligodendrocytoma 5%\n**Slow growing and relatively benign\n

*Those that can be voluntarily suppressed - [[Tics]]\n**[[Gilles de la Tourettes syndrome]]\n*‘Dance-like’ and unpredictable\n**[[Chorea]]\n*Fast, ‘shock-like’\n**[[Myoclonus]]\n*Large amplitude jerking movements\n**[[Ballismus]] – almost always unilateral so hemiballismus

*Very rare: incidence <1 per 100,000\n*Age of onset mean 4½ range 3-6\n*Language regression, usually to muteness\n*Behaviour disorder – many show autistic-like features\n*Due to continuous temporal lobe-centred focal/multifocal spikes, spike-waves during non-REM sleep, but equally frequent during REM sleep; paroxysmal abnormalities persist during over 90% of sleep\n*Both temporal lobes affected, even when there’s clearly a unilateral focus (origin)\n*The EEG disorder typically disappears during puberty\n*About 30% recover (much of) their language, 45% show improvement and 25% remain severely affected at 5-10 year follow-up\n*Treated with steroids or anticonvulsants. Occasionally surgery.\n*Overall long-term outcome strongly related to the duration of the untreated seizure disorder

*Variable – depending on site of lesion\n*[[Dysarthria]] and [[Dysphagia]] are common\n*Pseudo-bulbar palsy – resulting in a [[spastic dysarthria|Spastic Dysarthria]] is relatively common – due to bilateral lesions of articulatory motor cortex\n*[[Aphasia]] very variable\n

*Anomia\n*Due to semantic memory impairment\n*Topic shifts\n*Intrusions from hallucinations\n*Fluctuating performance\n

!General profile\n*Progressive loss of word and concept semantics\n**Particularly for low frequency words\n*Evident in word and picture definition, naming, reading with surface dyslexia (esp for low frequency irregular words)\n*Relatively well preserved: syntax, phonology, word and sentence repetition\n!Progression in naming errors\n*Close semantic errors - owl -> eagle\n*Superordinate errors - owl -> bird\n*More general errors - owl ->animal/cat\n*No responses\n!Left/Right balance\n*With more left than right atrophy performance worse with words than pictures\n*With more right than left atrophy performance worse with pictures than words \n!Site of pathology\n*Tissue loss is primarily inferolateral temporal cortex\n!Clinical diagnostic features\n*Semantic disorder (impaired understanding of word meaning and/or object identity) is the dominant feature initially and throughout the disease course. Other aspects of cognition, including autobiographic memory, are intact or relatively well preserved\n*I. Core diagnostic features\n*Insidious onset and gradual progression\n*Language Disorder characterized by\n**fluent, empty spontaneous speech\n**Loss of word meaning, manifest by impaired naming and comprehension\n**Semantic paraphasias \n*and/or perceptual disorder characterized by\n**1. Prosopagnosia: impaired recognition of identity of familiar faces and/or\n**2. Associative agnosia: impaired recognition of object identity\n*Preserved perceptual matching and drawing reproduction\n*Preserved single-word repetition\n*Preserved ability to read aloud and write to dictation orthographically regular words\n*II. Supportive diagnostic features\n*Speech and language\n**Press of speech\n**Idiosyncratic word usage\n**Absence of phonemic paraphasias\n**Surface dyslexia and dysgraphia\n**Preserved calculation\n*Behaviour\n**Loss of sympathy and empathy\n**Narrowed preoccupations\n**Parsimony\n*Investigations\n*Neuropsychology\n**Profound semantic loss, manifest in failure of word comprehension and naming and/or face and object recognition\n**Preserved phonology and syntax, and elementary perceptual processing, spatial skills, and day-to-day memorizing

*MS is a dynamic disease, with almost constant lesion formation and a progressive clinical course leading to physical disability\n*For every 8-10 new lesions detected on magnetic resonance imaging (MRI), only one clinical manifestation typically can be demonstrated\n*Patients with relapsing remitting MS have an average of 20 new lesions per year and one or two clinical exacerbations

*MEG: magneto-encephalography\n**completely noninvasive, non-hazardous technology for functional brain mapping, providing spatial discrimination of 2 mm and an excellent temporal resolution on the order of 1 ms \n**MEG measures the intercellular currents of the neurons in the brain giving a direct information on the brain’s activity \n**But only measures currents close to the surface of the brain\n**The fields produced are about 10-14 Tesla\n**One billionth smaller than the earth’s magnetic field\n***Need shielding\n***Detected by coils in a superconducting quantum interference device (SQUID) bathed in liquid helium at a temperature of -272°C

*It is an acquired autoimmune disorder characterized clinically by weakness of skeletal muscles and fatiguability on exertion. \n*Thomas Willis reported the first clinical description in 1672. \n

*Untreated MG carries a mortality rate of 25-31%\n*With current treatment, the mortality rate has declined to approximately 4%\n*Life expectancy is close to normal, but a substantial proportion of patients live with significant motor disability

*Uses a very strong magnetic field to polarise all the magnetic dipoles \n*Most of these are hydrogen ions – most common in water molecules\n*When the magnetic field is released, characteristic radiation signals are produced and detected\n*Essentially, MRI produces a map of water density\n*Involves very large magnetic fields. In clinical use typically 0.5-1.5 Tesla (5,000 to 15,000 Gauss), compared with the Earth’s magnetic field of 0.5 Gauss (ie 10,000 to 30,000x stronger). 3 Tesla machines are now routinely used for fMRI research, and 7 Tesla machines are coming into use.\n*Very strong magnetic fields appear to be safe, but long term follow up data may be needed!\n\n

*MS is caused by a disturbance in immune function\n*Cells of the immune system attack myelin, the insulating sheath that surrounds the nerve fibers (axons) located in the CNS (i.e., the brain and spinal cord)\n*When myelin is damaged, electrical impulses cannot travel quickly along nerve fibre pathways in the brain and spinal cord\n*Disruption of electrical conductivity results in fatigue and disturbances of vision, strength, coordination, balance, sensations, and bladder and bowel function\n

*When observed microscopically, plaques consist of inflammatory cells, astroglial cells, increased water (oedema), and destroyed myelin fragments\n*Larger plaques may be seen on magnetic resonance imaging (MRI) scans of the brain and spinal cord

*Most common cause of severe physical disability in young adults\n*2/3 of people with MS are ‘moderately or severely disabled’\n*Disability increases with disease duration \n**Over 80% significantly disabled after 20 yrs\n**Mean age of onset is ~30, so real disablement typically in 40s and 50s\n

[[Stroke]]\n[[Head Injury]]\n[[The Dementias]]\n[[Movement Disorders]]\n[[Multiple Sclerosis]]\n[[Motor Neurone Dx]]\n[[Myasthenia Gravis]]\n[[Seizure Disorders]]\n[[Tumours]]\n[[Infections]]\n[[Child Neurology]]\n[[Brain Imaging]]\n

*STM is normal\n*LTM\n**Impaired in verbal and non-verbal recall\n**Relatively unimpaired in recognition memory\n*So a retrieval difficulty\n**Retrieval poor for both recent and remote events\n

*An inflammation of the pia and arachnoid and underlying subarachnoid cerebrospinal fluid (CSF)\n*Acute - <1 day\n*Subacute - 1-7 days\n*Chronic - >7 days\n

*Supplies\n**[[Inferolateral frontal cortex]]\n**[[Superior and middle temporal gyri]]\n**[[Inferior parietal cortex]]\n**[[Insular cortex]]

*Important for language, but not currently clear how

*Tests\n**Orientation in time\n**Orientation in space\n**Memory\n**Attention\n**Language\n*Disproportionately emphasizes left hemisphere function

Found on the LHS of the heart (sending circulation to the body)

*[[Prevalence of MND]]\n*[[Damage and clinical signs in MND]]\n*Types of MND\n**Non-genetic\n***[[Amyotrophic lateral sclerosis (ALS) 65%]]\n***[[Progressive bulbar palsy (PBP) 25%]]\n***[[Progressive muscular atrophy (PMA) 8%]]\n***[[Primary lateral sclerosis (PLS) 2%]]\n*[[Dysarthria in MND]]\n*[[Aphasia and dementia in MND]]\n*[[Cause of MND]]\n*[[Progression of MND]]

*Controls\n**The leg

*The motor systems\n**[[Pyramidal system]]\n**[[Extrapyramidal system]]\n*[[Clinical tests for movement disorders]]\n*Movement disorders\n**[[Akinetic-rigid syndrome]]\n**[[Dyskinesia]]\n

*[[Prevalence of MS]]\n*[[MS is very disabling]]\n*[[MS is an autoimmune disease]]\n**[[Lesions in MS]]\n*[[MS is characterised by plaques on MRI scan]]\n*[[Symptoms of MS]]\n*[[Causes of MS]]\n*[[The course of MS]]\n**[[Factors affecting outcome]]\n*[[Diagnosis of MS]]\n*[[Treatment of MS]]

*Onset in 50s\n*May show:\n**Parkinsonian signs\n**Cerebellar signs\n**Pyramidal signs\n**With approximately equal frequency\n**Leads rapidly to death\n**Median time from diagnosis to death is 8 yrs.\n

*Muscle weakness that increases during periods of activity and improves after periods of rest\n*Muscles that control eye and eyelid movements, facial expression, chewing, talking, and swallowing are often, but not always, involved\n*The muscles that control breathing and neck and limb movements may also be affected\n*The first noticeable symptoms of myasthenia gravis may be \n**weakness of the eye or eyelid muscles 65%\n**difficulty in swallowing or slurred speech 16%\n**limb weakness 10% \n*The severity of weakness fluctuates during the day, usually being least severe in the morning and worse as the day progresses, especially after prolonged use of affected muscles \n

*[[MG is an acquired autoimmune disorder]]\n*[[Prevalence of MG]]\n*[[Muscle weakness is a feature of MG]]\n*[[Symptoms of MG]]\n*[[Dysarthria in MG]]\n*[[Dysphagia in MG]]\n*[[Cause of MG]]\n*[[The thymus in MG]]\n*[[The course of MG]]\n*[[Treatment for MG]]\n*[[MG prognosis]]

I.e., a heart attack, which causes scarring of heart tissue, and the development of thrombi

*Brief, arrhythmic, jerking, motor movements that last less than a second with a brief impairment of consciousness\n*Often cluster within a few minutes\n*If they evolve into rhythmic jerking movements, they are classified as evolving into a [[clonic seizure|Clonic seizures]]\n*Ictal EEG shows fast polyspike and slow wave complexes

*A brief, sudden, singular, shock-like muscle contraction - uncontrolled jerking when attempting to move\n*Sometimes generalised but may be focal\n*Difficult to distinguish from [[chorea|Chorea]]

contact me at neil dot barrett at gmail dot com\nIf you want

Email me, if you must, on neil dot barrett at gmail dot com

*After TBI, the brain is bathed with potentially toxic neurochemicals\n*Causes release of free radicals and breakdown of membrane lipids\n**These lipids fragment into mediators of inflammation\n*A cascade of processes is initiated, resulting in an increase in intraneuronal calcium and cell death\n*Neuroprotective drugs can inhibit these toxic neurochemical effects\n**No evidence for effectiveness in humans

*Now rare\n*Can mimic any other neurological disease\n*Tested for by Wasserman reaction on blood test\n

Not enough oxygen can also kill grey cells

*Inability to perform smooth pursuit in eye movements with saccades substituted

*Functions\n**Vision\n**Object recognition\n**Colour\n**Shape

*Swelling (cells take up water like a red bruise, not a black bruise)\n*Can be unilateral or diffuse, and can occur even in the absence of intracranial bleeding\n*Severe brain oedema probably occurs more often in children than in adults

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*Meningitis\n*Encephalitis\n*Seizure disorders (not usually acquired)\n*Tumours\n* … almost any adult disorder can occur in childhood\n*(And then there are the ‘autistic spectrum disorders’ – but possibly not neurological)\n

!Stroke and death\n*17-34% of people die within the first month. This is strongly related to:\n**Length of time unconscious\n***>24 hours is not good\n**Age\n***Older people have other diseases as well, for a start\n**Concomitant heart disease and hypertension\n*1 year fatality rate of 33%\n**Usually after a second stroke\n----\nIt is hard to identify a fair sample of all types of stroke - some are just treated by doctors, some don't get treated at all!\n!Long term outcome\n*1-25% can return to work (depends what you mean by work)\n*50-75% can walk unaided and are discharged home\n*20-30% require long term institutional care\n*30-50% have difficulties feeding themselves\n*70% return to the community

*PET: positron emission tomography\n*Uses very short half life radioactive materials – eg O15 whose half-life is 2 minutes\n*Because of the very short half life, a cyclotron is needed on site to make the unstable radioactive elements.\n*O15 labelled ~CO2 is injected/breathed in and enters the blood stream.\n*The amount in the brain tissues reflects the amount of blood flow that piece of brain is getting.\n*The labelled element decays by emitting a positron. This travels a short distance until it hits and is annihilated by an electron, producing 2 γ rays that go in opposite directions.\n*A circular detector around the head detects simultaneous arrival of γ rays and their source is determined.\n*Blood flow can be measured across the whole brain\n*A series of scans can be carried out on a person with a 10 minute interval (typically 6-18 in a session)\n*Blood flow measured over a period of 30-45 secs\n*Can look for changes in rCBF between different conditions\n*PET can detect changes of 2-3% in rCBF\n*PET: image processing\n**Brains are normalised: transformed into a standard shape (The Talaraich space)\n**Then blood flow measurements are smeared\n**Resolution is now around 20mm \n

!Incidence\n*1 per 1000\n*Rare below 50yrs: increases with age – 1.5% between 70-79 and 3.5% over 80\n!What is Parkinsons?\n*TRAP\n**[[Tremor]]\n**Rigidity\n**Akinesia (or bradykinesia)\n***Lack of or slow movement\n**Postural instability\n!Early symptoms\n*Stiffness\n*Difficulty in initiating fine movements esp writing\n*Fatigue\n*Sometimes tremor \n!Characteristics\n*Rest tremor\n**Coarse and slow \n**Mainly affects hands – pill-rolling tremor \n*Cogwheel rigidity (lead pipe rigidity)\n**Due to intermittent increase in tone \n*Face\n**Immobile, greasy skin\n*Fast repeated movements\n**Slow up – bradykinesia/festination\n**Slowness of voluntary movement with progressive reduction in speed and amplitude of repetitive actions \n*Posture\n*Loss of arm swing, short steps\n!Language profile and cognition\n*[[Dysarthria]]\n**Is frequent, with loss of intonation, slow initiation, festinating speech\n*Writing\n**Micrographia\n*Dementia\n**Occurs in the later stages in around 30% of patients\n**Very similar to dementia with Lewy bodies (DLB)\n*[[Treatment of Parkinson's diseaase]]

*Depends on what artery / branch of artery is effected\n**Anterior branch of [[Middle cerebral artery (MCA)]]\n***[[Broca's aphasia]] in dominant hemisphere\n***Neglect in non-dominant hemisphere\n***Contralateral hemiparesis, particularly of face and arm\n**Posterior branch of [[Middle cerebral artery (MCA)]]\n***Fluent aphasia in dominant hemiphere (owing to loss of [[Wernicke's area]])\n***Constructional apraxia in non-dominant hemisphere\n**[[Anterior cerebral artery (ACA)]]\n***Hemiparesis of leg more than arm\n***Dysexecutive syndrome - typically in acute stage: apathy and incontinence

*[[Simple partial seizures]]\n*[[Complex partial seizures]]\n*[[Secondarily generalised seizures]]

*incidence 1 in 5000 live births\n*results in\n**58% cerebral palsy \n**39% seizure disorders percent had epilepsy \n**25% delayed/disordered language \n**22% behavioural problems (e.g. hyperactivity) \n

*Result in raised intracranial pressure\n*Resulting, chronically, in headache, vomiting, and reduced consciousness (drowsiness, or coma).\n*Usually with cerebral oedema\n*Or hydrocephalus\n**Where the tumour obstructs CSF drainage\n

*Contusion results in [[oedema|Oedema]]\n*Both [[haemorrhage|Haemorrhage]] and [[oedema|Oedema]] result in raised intracranial pressure\n*Raised intracranial pressure results in hypotension\n*Both result in cerebral ischaemia\n*Which in turn causes further oedema...

*Pick's disease is defined pathologically by severe atrophy, neuronal loss, and gliosis, disproportionately affecting the frontal and temporal cortical regions. \n*Histology shows:\n**Swollen (ballooned) neurons (Pick cells) \n**Argentophilic (= argyrophilic = staining with silver) neuronal inclusions known as Pick bodies\n*Leads to a brain with knife-like gyri\n

*90% of patients with [[Wernicke's aphasia]] have lesions affecting [[Wernicke's area]]\n*48% of patients with lesions affecting [[Wernicke's area]] have [[Wernicke's aphasia]]\n*59% of patients with [[Broca's aphasia]] have lesions affecting [[Broca's area]]\n*24% of patients with lesions affecting [[Broca's area]] have [[Broca's aphasia]]\n//Willmes & Poeck, 1993//\n*Few patients with [[Conduction aphasia]] have lesions affecting the [[Arcuate fasciculus]]\n*Lesions in many areas outside the classical language areas can result in aphasia\n**[[Ventrolateral temporal lobe or Infero-lateral temporal cortex or basal language area]]\n**[[Subcortical lesions]]\n**[[Thalamic lesions]]

*Follows unconsciousness\n*A confusional state\n*Suffering severe anterograde amnesia\n*Duration is 4 times the duration of unconsciousness\n*Duration is strongly associated with outcome\n**<1 hour - 90% of patients at work in 2 months\n**>24 hours - 80% of patients return to work in 6 months

*Supplies\n**[[Occipital lobe]]\n**[[Ventrolateral temporal lobe or Infero-lateral temporal cortex or basal language area]]\n**[[Ventromedial temporal lobe]]\n**[[Superior parietal lobe]]\n**[[Brain stem]]\n**[[Cerebellum]]

*Large vessels:\n**[[Vertebral arteries]]\n**[[Basilar artery]]\n**[[Posterior cerebral artery]]\n*Small vessels\n**Branches from all these

*Contralateral homonymous hemanopia (owing to loss of the [[occipital lobe|Occipital lobe]])\n*Contralateral sensory loss\n*Memory impairment (owing to loss of the [[ventromedial temporal lobe|Ventromedial temporal lobe]])\n*Naming impairment (owing to loss of the [[Ventrolateral temporal lobe or Infero-lateral temporal cortex or basal language area]])\n*See also [[basilar artery|Basilar artery]] for basilar artery infarcts

*A variable period of unconsciousness during which the patient becomes quiet and breathing resumes\n*The patient gradually awakens, often after a period of stupor or sleep, and is confused, with some automatic behavious\n**Such as plucking at the arms and lip smacking\n*Headache and muscular pain are common\n*The patient does not recall the seizure itself

*Severe head injury with haematoma or PTA>24 hours brings a 12% risk of epilepsy over 5 years\n*Moderate head injury with skull fracture or PTA>30 minutes bring a 1.6% risk of epilepsy over 5 years

*Very common, may occur in 30-80% of patients after a head injury\n*After severe head injury, they are //less// frequent than in the normal population

*[[Tremor]]\n*[[Dystonia]]\n*[[Parkinsonism]]\n----\n*2 year follow up - 12% had persistent movement disorders - Parkinsonism most rare

*Disorders of emotional functioning are often documented\n**Major depression occurs in 44% of patients after head injury\n***Depression has been associated with left frontal injuries\n**Bipolar disorder is also more frequent in patients with head injuries\n**Impulsivity and disinhibition as a result of [[frontal damage|Frontal lobe syndrome]]

*Poorer with\n**Cough after swallow (indicates aspiration)\n**Voice change after swallow\n**Abnormal voluntary cough\n**Abnormal gag reflex (but only about 60% of normal people have one!)\n**Dysphonia\n**Dysarthria\n*Unrelated to\n**Laterality or location of lesion\n**[[Aphasia|Aphasia post stroke]]\n**Neglect

*Controls\n**Executive functions

*Prevalence c 14/100,000 population\n*Women used to be more often affected than men (3:2). \n*The most common age at onset is the 20-40 in women and the 70-90 in men. \n*As the population ages, the average age at onset has increased, and now males are more often affected than females, and the onset of symptoms is usually after age 50. \n

*One of the most common neurodegenerative diseases of adult onset; 1-2 per 100,000\n*Predominantly affects middle aged and elderly people with a mean age of onset of 55 years\n**younger people occasionally affected. \n*Is sporadic in 90% of cases, but about 10% are familial, usually with an autosomal dominant mode of inheritance

* Sussex - 111 per 100,000\n* Orkney - 258 per 100,000

*Treat hypertension\n*Smoking\n*Weight\n*Exercise\n*Blood cholesterol\n*Low dose aspirin not recommended for primary prevention\n**Although it probably wouldn't do any harm

*Only ~UMNs affected\n*Progressive upper motor neurone syndrome with limb spasticity and weakness accompanied in time by a [[pseudobulbar palsy|Pseudobulbar palsy]]

*Premonitory symptoms occurring hours or days before the seizure\n*Common prodromes include: mood changes, sleep disturbances, lightheadedness, anxiety, irritability, difficulty concentrating\n*And rarely, an ecstatic feeling\n*Prodromes, which are generalised, non-localised feelings, can be part of a generalised seizure\n*An aura represents a simple partial seizure, and therefore is not a part of a generalised seizure\n**Simple partial seizures can develop into generalised seizures\n\n

*Death - mortality rate of severe head injuries is 25-36% in adults within the first 6 months after injury\n*[[Vegetative state]]\n*Partial recovery\n*Full return to work - 82% of patients with mild or moderate head injury experienced a good 1 year outcome, and 73% were able to return to work\n----\n*Most important prognostic factors\n**Mechanism of injury \n**Postrecuscitation GCS score\n**Postrecuscitation pupillare reactivity\n**Postrecuscitation blood pressure\n**Intracranial pressures\n**Duration of PTA\n**Sitting balance\n**Intracranial pathology identified on neuroimaging

*50% die in 3-4yrs\n*20% live for 5 yrs\n*10% live for 10 yrs\n

*Start as isolated and progressive language impairments\n*Often first noticed as a difficulty with peoples’ names – and misdiagnosed as AD\n*In the long term – which can be quite long – progresses to a generalised dementia\n*Typical age of onset is 45-60 (like FTD but much earlier than is typical in AD, VD and DLB that typically have onset after 60).\n

*Symptoms begin in muscles controlling speech, chewing and swallowing controlled by nuclei in the pons and medulla\n*About 25% of cases at onset, especially women\n*Progressive dysarthria and dysphagia\n*Limb, neck and trunk involvement later\n*Usually show mixed UMN and LMN features although one type may predominate\n

*Affects purely the lower motor neurones\n*Resulting in progressive weakness and atrophy

*Probably two varieties:\n**(i) characterised by phonological errors in speech production\n**(ii) characterised by syntactic difficulties\n*Related to inferolateral frontal degeneration\n*Often, but not necessarily, accompanied by other frontal symptoms (personality change, mood change, executive disorder) \n*Subvariety of [[FTD - Frontal Variant|Fronto-temporal dementia - Frontal variant]]?\n

*Early signs\n**Unsteadiness and falls\n**[[Dysarthria]] “quiet and spastic” \n**Eye movement difficulties common\n**Memory impairment/personality change\n**Little effective treatment\n**Evidence of subcortical degeneration

*Depression in the elderly can often be confused with dementia\n*Around 10% of people diagnosed with dementia are later reclassified to depression\n**Depression is reversible, and not progressive

*The characteristic features are:\n**apparent weakness of the muscles of mastication - V - and facial expression - VII - presenting with difficulty in chewing and an expressionless face. The jaw jerk is exaggerated. \n**spastic dysarthria –husky or gravelly voice \n**palatal weakness and difficulty in swallowing: hypernasal voice - X \n**brisk gag reflex - IX, X cranial nerves \n**tongue is immobile, pointed and cannot protrude - XII - this should be discriminated from the slow moving tongue seen in Parkinsonian patients \n*Sometimes: \n**emotional lability - increased emotions with unprovoked outbursts of laughing or crying \n**bilateral limb upper motor neurone signs

*Upper motor neurones (Betz cells/Pyramidal cells) decussate & run to:\n**Lower motor neurones in ventral horn of spinal cord and motor cranial nerve nuclei\n*Controls\n**Voluntary, conscious movement\n**The extent and force of movement\n*Lesions\n**To upper motor neurones cause spasticity (rigidity, increased tone)\n**To lower motor neurones cause flaccidity and weakness\n

*Head injury\n**Around 3% of cases\n**Especially when severe\n**Especially when due to penetrating injury\n*Tumours\n**Around 10% of cases\n**More often in the elderly\n**40% of tumours have seizures as first symptom\n*CVA\n**Much more frequent after [[haemorrhagic stroke|Haemorrhage]] (around 25%) than [[ischaemic/embolic stroke|Infarction or ischaemic stroke]] (4%)\n*CNS infections\n**[[Meningitis]] / [[Encephalitis]]\n**Risk around 6%\n**Higher after viral encephalitis\n!In summary\n*Any CNS 'insult' results in a raised risk of developing some form of epilepsy\n

!Increasing cerebral blood flow\n*Done by decreasing arterial spasm\n*Experimental procedure - risks currently seem to outweigh benefits

*Poor at pragmatic inference: jokes, similies, inference in general\n*Poor at comprehension and / or production of intonation

!Advancing age\n*Incidence increases geometrically with age\n*Under 50: <1 per 1000 people per annum\n*Age 70: 9 per 1000\n*Age 80: 20 per 1000\n*Stroke does occur in childhood, but much less frequently\n**Usually there are different causes\n\n!Other risk factors\nAs stroke is a cardiovascular disease, many risk factors are related to the heart\n----\n*Hypertension\n*Arteriosclerosis / high cholesterol (hardening of the arteries)\n*Heart disease, especially valve disease, infectious endocarditis\n*Previous stroke or TIA and / or family history (no evidence that this is genetic)\n*Diabetes (associated with heart disease and a poor diet)\n*Unhealthy diet\n*Sickle cell disease\n*Smoking (associated with hypertension)\n----\nTo some extent it is a disease of poverty

*Around 10% of AD is familial\n*Risk is around 3.5 times higher if a first degree relative has dementia\n*TBI with loss of consciousness - 80% increase in risk\n*Smoking results in a 20% decrease in risk of developing AD

*Use of anticoagulants and antiplatelet medications (such as aspririn) raise the risk of intracranial bleeding with even trivial head injuries\n*Alcohol use raises the risks of incurring a head injury\n**May impede excitotoxicity - so it may actualy decrease liklihood of a poor outcome!\n**Patients consuming alcohol have higher initical [[GCS]] scores\n**People who are drunk fall in a more relaxed way, which is good for outcomes too!

*SPECT: single proton emission computerised tomography\n*Uses a single dose of long half-life radioactive compound\n*Imaging takes a picture of its distribution in the brain, by detecting the radioactive decay\n*Usually used to detect a pattern of oxygen utilisation – metabolism in the brain – but can detect the distribution of a variety of things\n*Poor spatial resolution – smeary image – but shows what isn’t working\n\n

*Sudden Death in Epileptic People\n*80% occur during or immediately after a seizure\n*Most likely due to respiratory obstruction or cardiac arrest\n*Accounts for 8-17% of deaths of people with epilepsy

*Any pathway to a [[GTCS|Tonic-clonic seizures (grand mal)]] is possible\n*Often begin with an aura that evolves into a complex partial seizure, and then into a generalised tonic-clonic seizure\n*There may not be an aura, or there may not be a complex partial seizure

*An abnormal paroxysmal discharge of cerebral neurons due to cortical hyperexcitability\n*[[Incidence and prevalence of seizures]]\n*Cross classified by\n**Seizure type\n***[[Generalised seizures]]\n***[[Partial seizures]]\n***[[Childhood febrile seizures]]\n***[[Status epilepticus]]\n***[[Temporal lobe epilepsy]]\n**[[Aetiology|Aetiology of seizures]]\n*[[Treatment of seizures]]\n

*On scalp EEG recordings, they may appear to start simultaneously in both cerebral hemispheres\n**As no one hemisphere is unaffected, unconsciousness is inevitable\n*Probably begin in the thalamus and other subcortical structures\n*A seizure results from a paroxysmal high voltage electrical discharge of susceptible cerebral neurons within an [[epileptogenic focus|Epileptogenic focus]]\n**When these neurones overcome the surrounding inhibitory influence, the seizure discharge spreads to neighbouring cortical structures and then to subcortical and brainstem structures\n*EEG\n**Generally normal between fits (interictal EEG)\n**In the tonic phase - progressively higher amplitude and lower frequency discharge pattern\n**Then becomes slower and mixed with bilateral high-amplitude spikes and a progressively greater amount of high-amplitude rhythmic delta activity\n*To record a seizure on an EEG (in order to rule out [[Pseudoseizures]])\n**It may be necessary to implement sleep deprivation or photic stumulation

*Naming impairment particularly for low frequency words\n*Difficulty with word comprehension\n*Difficulty with semantic judgements (eg Pyramids and Palm Trees)\n*[[Surface dyslexia]]\n*Due, probably, to inferolateral temporal tissue loss – the [[‘basal language area’|Ventrolateral temporal lobe or Infero-lateral temporal cortex or basal language area]]

*Caused by there being a fixed foramen magnum and brain scraping on temporal bone\n*Typically damage to hippocampus - memory

*Is due to a genetic abnormality of haemoglobin\n*Tends to ‘clump’ when deoxygenated\n*Due to a recessive gene\n*That is relatively common in people with West African ancestry (much lower proportions in Eastern Mediterranean and Indian aboriginal populations)\n*Normal red cells maintain their shape as they pass through the capillaries and release oxygen to the peripheral tissues (upper panel). Haemoglobin polymers form in the sickle cells with oxygen release, causing them to deform. The deformed cells block the flow of cells and interrupt the delivery of oxygen to the tissues (lower panel). \n*Results in a high rate of childhood stroke\n*4% of people with SSD have stroke \n*Both thrombotic (c68%) and haemorrhagic stroke\n*Mechanism of cause not clear\n*Median age 5yrs

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!Symptoms (what people complain about)\n*Sudden numbness or weakness of the face, arm, or leg, especially on one side of the body\n*Sudden confusion, difficulty in speaking or understanding\n*Sudden deterioration of vision of one or both eyes\n*Sudden difficulty in walking, dizziness, and loss of balance or coordination\n*Sudden, severe headache with no known cause\n//American Stroke Association//\n!Signs (what you can test and demonstrate)\n*These are variable - depending on where the stroke has occurred.\n!FAST test\n*Facial weakness - can the person smile?\n*Arm weakness - can the person raise both arms?\n*Speech problems - comprehension and production okay?\n*Test all three symptoms - if they fail one, phone 999

*A seizure with preservation of consciousness\n*Many kinds\n**Sensory\n**Motor\n**Autonomic\n**Psychic experiences\n*Any discrete human experience involving the cerebral cortex could be a simple partial seizure\n*Diagnosis based on\n**Repeated stereotypic occurrence of the same experience\n**Associated with focal EEG changes\n**Diagnosed after a recurrent aura leads to a complex partial seizure or a secondarily generalised seizure\n**Disappearance of the recurrent experience, with anticonvulsants supporting the diagnosis

In the last minute stylee

Neurology revision

*Complete or partial occlusion of arteries\n*Blockage of small arteries by [[microatheroma]] and other vessel diseases\n*Nearly always related to hypertension\n*Because lesions are typically small, it has a good prognosis, typically effects are temporary\n*Shows up as little white dots on an MRI scan\n*Effects\n**Pure motor hemiparesis (usually an internal capsule lesion)\n**Pure sensory stroke (usually thalamic lesion)\n**Ataxic hemiparesis\n**Dysarthria / clumsy hand syndrome\n**Sensorimotor stroke

See [[Spastic hemiplegia]]

*CP: spastic hemiplegia and diplegia\n*May have:\n**epilepsy\n**mild to moderate learning disability\n**speech rarely affected\n**Language disorder typically consonant with degree of learning disability\n\n

*Usually severely dependent\n*Often severe learning difficulties\n*With very delayed language\n*And dysarthria and dysphagia\n*Seizures also common\n

*[[Dysarthria|Dysarthria post stroke]]\n**Cerebellar\n**Bulbar palsy (result of lesion to the [[brain stem|Brain stem]])\n**Pseudobulbar palsy (result of a [[motor cortex|Motor cortex (superior)]] lesion)\n*[[Aphasia|Aphasia post stroke]]\n*[[Articulatory apraxia]]\n*[[Dysphagia]]

*[[Dysphagia]]\n*[[Dysarthria]]\n**Both of these are frequent because of the shearing action on the base of the brain\n*[[Aphasia]]\n**Relatively rare\n**Perisylvian regions are usually relatively undamaged as they are not peripheral\n**Bilateral [[temporal pole|Temporal pole]] damage results in a fluent jargon aphasia

*A neural tube defect involving incomplete development of the brain, spinal cord, and/or their protective coverings\n*caused by the failure of the fetus's spine to close properly during the first month of pregnancy\n*Infants born with SB sometimes have an open lesion on their spine where significant damage to the nerves and spinal cord has occurred. \n*the spinal opening can be surgically repaired shortly after birth, but the nerve damage is permanent, resulting in varying degrees of paralysis of the lower limbs\n*Even when there is no lesion present there may be improperly formed or missing vertebrae and accompanying nerve damage. \n*About 0.4 per 1000 births: declining rate\n*Results in physical and mobility difficulties\n*Nearly always some form of learning disability with delayed language development\n*SB may also cause bowel and bladder complications\n*many children with SB have hydrocephalus

*Hours/days\n**Tissue reperfusion\n*Days/weeks\n**Reorganisation of structure - function relationships\n*Weeks/years\n**Establishing new pathways and compensatory mechanisms

*A seizure lasting at least 30 minutes, either continuously, or intermittently\n*Any type of seizure can move into status\n*With [[GTCS|Tonic-clonic seizures (grand mal)]] status can be life-threatening\n*Seizures are typically stopped with a benzodiazapine

*[[What is a Stroke]]\n**[[Signs and Symptoms of Stroke]]\n**[[Incidence and Prevalence of Stroke]]\n**[[Outcomes of Stroke]]\n**[[Risk Factors for Stroke]]\n**[[Primary Stroke Prevention]]\n*[[Types of Stroke]]\n*[[Stages of Stroke Recovery]]\n**[[Acute Stroke Treatment]]\n**[[Chronic Stroke Rehabilitation]]\n*[[Effects of Stroke]]\n**[[Anatomy of the Blood Vessels]]\n*[[Stroke Classification]]\n*[[Speech and Language Disorders Post Stroke]]\n**[[The Neo-classical Story]]\n**[[Articulatory disorders]]\n**[[Swallowing disorders]]

*[[Total anterior circulation stroke (TACS)]] \n*[[Partial anterior circulation stroke (PACS)]] \n*[[Posterior circulation stroke (PCS)]]\n*[[Lacunar stroke|Small Vessel Disease or Lacunar Stroke]]\n*[[Haemorrhage]]\n**[[Intracerebral]]\n**[[Subarachnoid|Subarachnoid Haemorrhage]]\n**[[Subdural]]

!Location of Haemorrhage\nMost likely to happen at the Circle of Willis, as this is where the blood pressure is highest\n*Anterior cerebral artery - 40%\n*Posterior communicating artery - 30%\n*Middle cerebral artery - 20%\n*Basilar artery - 10%\n!Causes\n*Aneurysm arises from a weakness in the wall of a vessel\n**Eventually this bursts\n***Surgery - clipping the aneurysm, preferably before a bleed\n*An AV malformation\n**Large vessels link arteries to veins\n***This deprives surrounding tissues of oxygen\n***Also liable to develop aneurysms because the large blood vessels are weak

Between the arachnoid layer and the pia mater\nSee [[Cerebral Membranes]]

*Often small lesions\n*Resulting in, typically mild [[aphasia|Aphasia post stroke]] with a good prognosis\n*Recent evidence suggests that the aphasia is due to ischaemia in overlying cortex\n*When the ischaemia is reversed, the aphasia is reversed

Between the dura and the arachnoid layer\nSee [[Cerebral Membranes]]

*Incorporates\n**[[Heschl's gyrus]] - primary auditory cortex\n**[[Wernicke's area]] (in dominant hemiphere)\n**[[Temporal pole]]\n**[[Middle temporal gyrus]]

*Functions\n**Important for the spatial location of objects\n*Damage leads to\n**Neglect\n**Constructional problems\n**Left-right disorientation\n**Dyscalculia

*Lies anterior to the motor cortex, right at the top of the frontal lobe\n*Lesions typically result in a short-lasting articulatory difficulty

*Lesioned in patients with STM impairment\n*Other inferior parietal lesions also lead to STM impairment

*Where you make regularisation errors

*Aim is to remove the epileptic focus, or to disconnect it\n**Without removing any cortical tissue essential for any cognitive (or motor or sensory) function\n***There is particular concern over avoiding cortex important for language and memory\n*Only worth considering in people with intractable and disabling chronic epilepsy\n*68% involve temporal lobe excisions\n*24% other cortical excisions\n*6% corpus callosotomy\n*2% hemispherectory

*35-50% of stroke patients have [[dysphagia|Dysphagia]]\n*More than 80% recover completely within four weeks (but about 50% have abnormalities on videofluoroscopy)\n*Common after brain stem strokes that affect the nuclei of the nerves involved\n*Also common after cortical stroke\n**Left hemisphere is dominant for swallowing for 63% of people (30% right hand side, 7% equal dominance)\n**Bilateral cortical innervation means that recovery is usual after unilateral cortical stroke

*Vary in type and severity, \n*May include:\n**a drooping of one or both eyelids (ptosis)\n**blurred or double vision (diplopia) due to weakness of the muscles that control eye movements\n**unstable or waddling gait\n**weakness in arms, hands, fingers, legs, and neck\n**a change in facial expression\n**difficulty in swallowing\n**shortness of breath\n**dysarthria

*Symptoms vary - depending on the nerve fibre pathways involved\n*Tingling is a result of loss of myelin in the spinal cord\n*Urinary incontinence is a result of damage to the nerve fibres to the bladder\n*Imbalance or incoordination may result from damage to the nerve fibres in the cerebellum\n*[[Table of symptoms and frequencies in MS]]\n*[[Articulatory impairment in MS]]\n*[[Memory impairment in MS]]

|!Symptom|!Frequency|\n|Fatigue|77%|\n|Balance problems|74%|\n|Weakness or paralysis|63%|\n|Numbness, tingling or other sensory impairment|63%|\n|Bladder problems|59%|\n|Spasticity|49%|\n|Bowel problems|39%|\n|Memory problems|37%|\n|Emotional lability|32%|\n|Visual impairment|30%|\n|Tremor|27%|\n|Speech and/or communication difficulties|23%|\n|Difficulty solving problems|21%|

*Simple partial seizures without loss of awareness (with or without aura), or\n*Complex partial seizures - loss of awareness owing to the seizure spreading to involve both temporal lobes, which causes impairment of memory\n*Aura - short phase\n**Olfactory and gustatory hallucinations\n**Auditory hallucinations consist of a buzzing sound, a voice or voices, or muffling of ambient sounds\n**Visual illusions including distortions of shape, size and distance of objects\n**Depersonalisation\n**Deja vu or jamais vu\n**Fear or anxiety (usually associated with seizures arising from the amagdala)\n**Sense of dissociation or autoscopy\n*Temporal lobe complex partial seizure begins - typically seconds or minutes long\n**Wide-eyed motionless stare, dilated pupils and behavioural arrest\n**Oral automatisms may be noted\n**Manual automatisms may also be observed\n*Complex partial seizure may evolve to a secondarily generalized tonic-clonic seizure\n*There is usually a postictal period of confustion (this distinguishes TLE from absence seizures) - lasting a longer period (several minutes)\n*Postictal aphasia suggests onset in the language-dominant temporal lobe\n!Treatment\n*Best results from temporal lobe excisions\n*Necessary to limit the excisions in the dominant temporal lobe\n*[[Wada test]] enables neurologist to determine which hemisphere is dominant\n**Other methods include carotid doppler sonography, PET, SPECT or ~fMRI (measuring regional cerebral blood flow during language tasks), implanted subdural electrodes, and intraoperative cortical stimulation\n*Complications of temporal lobectomy\n**Death - <0.5%\n**Persistent hemiplegia - 2%\n**Persistent aphasia - 1%

*? Important for sentence and text comprehension

*Small lesions\n*Thalamus has massive connections to overlying cortex\n*[[Aphasia|Aphasia post stroke]] typically fluent and anomic, with good repetition

[[What is dementia]]\n[[Varieties of dementia]]\n[[Pseudo dementia]]\n[[Dementia comparison table]]

*Neo-classical classification\n**[[Broca's aphasia]]\n**[[Wernicke's aphasia]]\n**[[Conduction aphasia]]\n**[[Global aphasia]]\n**[[Transcortical motor aphasia]]\n**[[Transcortical sensory aphasia]]\n*[[Neo-classical Aphasias comparison table]]\n*[[Poblems with the Neo-classical story]]

*The medullary swallowing centre\n*Receives sensory input, from V, VII, IX, X\n*Receives input from motor cortex bilaterally\n*Controls the pharyngeal and oesophageal phases of swallowing\n*The oral phase is under voluntary cortical control

*Variable but usually progressive \n*Weakness is restricted to the ocular muscles in about 10% of cases \n**The rest have progressive weakness during the first 2 years that involves oropharyngeal and limb muscles \n*Maximum weakness occurs during the first year in two-thirds of patients \n*Before corticosteroids were used for treatment, approximately one-third of patients improved spontaneously, one-third became worse, and one-third died of the disease\n*Spontaneous improvement frequently occurred early in the course\n*Symptoms fluctuated over a relatively short period of time and then became progressively severe for several (~3) years (active stage)\n*The active stage is followed by an inactive state in which fluctuations in strength still occurred but are attributable to fatigue, intercurrent illness, or other identifiable factors\n*After 15 to 20 years, weakness often becomes fixed and the most severely involved muscles are frequently atrophic (burnt-out stage)\n*Factors that worsen myasthenic symptoms are emotional upset, systemic illness (especially viral respiratory infections), hypothyroidism or hyperthyroidism, pregnancy, the menstrual cycle, drugs affecting neuromuscular transmission, and increases in body temperature

*At onset:\n**Relapsing-remitting c 65%\n**Progressive course with superimposed acute episodes c15%\n**Progressive course c20%\n***Most develop into progressive\n***41% by 10 years, 57% by 15yrs and 65% by 25yrs\n***Around 10% stay with relapsing-remitting – relatively benign\n*On average 25 years from diagnosis to residential care\n*But life expectancy only reduced by 7 years in MS\n*For most people with MS, increasing disability and dependence \n\n

*In adults with myasthenia gravis, the thymus gland is abnormal. It contains certain clusters of immune cells indicative of lymphoid hyperplasia - a condition usually found only in the spleen and lymph nodes during an active immune response. Some individuals with myasthenia gravis develop thymus tumours. Generally thymomas are benign, but they can become malignant\n*The relationship between the thymus gland and myasthenia gravis is not yet fully understood. The thymus may give incorrect instructions about the production of the acetylcholine receptor antibodies, thereby setting the stage for the attack on neuromuscular transmission

*Complete or partial occlusion of arteries\n*Associated with increased blood pressure and cholesterol\n*Due to atherosclerosis: deposition of lipds in smooth muscle cells in the wall results in [[stenosis]]\n*Stenosis leads to slow flow with development of thrombosis\n*Atherosclerosis results in an [[ulcer|Arterial Ulcer]] on the artery wall, with laying down of fibrin, platelet adhesion, trapping of blood cells\n*It is a vicious circle - the more the clot, the slower the flow, the more the clot...\n*So a blod clot blocks the artery\n

*Can be voluntarily controlled\n*Fragments of normal movements\n*Include vocal tics, usually sniffs, throat clearing and swearing

*Generalised convulsive seizure may begin with [[myoclonic jerks|Myoclonus]], or rarely, with [[absences|Absences (petit mal)]]\n*The tonic phase begins with flexion of the trunk and elevation and abduction of the elbows\n*Subsequent extension of the back and neck is followed by extension of arms and legs\n*This can be accompanied by apnoea, which is secondary to laryngeal spasm\n*You don't wet yourself at this stage\n*This stage lasts for 10-20 seconds

*Sudden-onset tonic extension or flexion of the head, trunk, and/or extremities for several seconds\n*Typically occur in relation to drowsiness, shortly after falling asleep, or just after awakening\n*Often associated with other neurologic abnormalities\n*Ictal EEG shows an 'electrodecremental' response - a beta buzz of relatively low amplitude

*20-25% of cases of epilepsy\n*Composed of (textbook definition)\n**[[Prodromal phase: "aura"]]\n**[[Tonic phase: tonus]]\n**[[Clonic phase: clonus]]\n**[[Postictal stage: stupor]]\n*Now accepted however that if there is an aura, then it is not a tonic clonic seizure

*Taking out all of the [[anterior|Anterior cerebral artery (ACA)]] and [[middle|Middle cerebral artery (MCA)]] cerebral arteries of one side\n*This leads to the loss of all of the [[frontal lobe|Frontal lobe]] and some [[parietal lobe|Parietal lobe]]\n*A result of occlusion of the [[internal carotid artery|Internal carotid artery]]\n*Effects\n**Dense flaccid hemiparesis affecting arm, face and leg\n**Homonymous hemianopia - loss of visual field on the side contralateral to the lesion\n**Global aphasia, if dominant hemisphere\n**Inattention or neglect if non-dominant hemisphere\n**High mortality and severe long term morbidity\n

They break down, contents bathe surrounding cells in toxic fluid\nGlial cells will gobble up nasty dead bits

*Disconnection of [[Broca's area]] from (distributed) semantics\n*Non-fluent speech production\n*Good repetition\n*Good auditory comprehension

*Disconnection of [Wernicke's area]] from (distributed) semantics\n*Fluent paraphasic speech production\n*Good repetition\n*Poor auditory comprehension

*Attempts to find treatments not very conclusive\n*AD results in a depletion of acetyl choline\n*Some evidence that acetyl cholinesterase inhibitors – such as aricept or rivastigmine – can slow or halt disease progression, particularly in people with early onset AD\n*Behavioural treatment\n**Teaching/encouraging use of memory strategies\n**Diaries, reminders\n**Cueing books – eg of friends and relatives\n**Reality orientation therapy\n**Carer support\n\n

!Corticosteriods\n*Marked improvement or complete relief of symptoms occurs in more than 75% of patients treated with prednisone\n*Some improvement occurs in most of the rest. \n*Much of the improvement occurs in the first 6 to 8 weeks, but strength may increase to total remission in the months that follow \n!Cholinesterase Inhibitors\n*Retard the enzymatic hydrolysis of ~ACh at cholinergic synapses, so that ~ACh accumulates at the neuromuscular junction and its effect is prolonged\n*cause considerable improvement in some patients and little to none in others\n*Strength rarely returns to normal \n!Thymectomy\n*Is recommended for most patients with early onset \n*the maximal response generally occurs 2 to 5 years after surgery. \n*the response is relatively unpredictable and significant impairment may continue for months or years after surgery\n*best responses to thymectomy are in young people early in the course of their disease \n*patients with disease onset after the age of 60 rarely show substantial improvement from thymectomy \n

*Because of the executive problems, people with DLB are hard to manage. They wander, get lost, get paranoid about their hallucinations etc. Because their episodic memory is relatively well preserved the severity of their disorder is often not fully appreciated\n*The behavioural difficulties are often treated with major tranquilisers eg chlorpromazine\n**This results in rapid worsening of the dementia, and, often, the development of [[Parkinsonian|Parkinsonism]] features\n

*Immunomodulating drugs\n**β-interferon (and copaxone) slow the progression of RR MS\n**β-interferon may also work in secondary progressive MS\n*Immunosuppressive drugs\n**Little evidence of effectiveness\n*Corticosteroids\n**Improve short term recovery after a relapse\n**Have no long term effects\n*Cannabis\n

!Drug treatment\n*Primarily with Levo-dopa\n**Yields dopamine that is deficient in PD\n**And with a variety of dopamine agonists that increase or potentiate dopamine production\n!Surgery\n*Thalamotomy and thalamic stimulation\n*Pallidotomy and pallidal stimulation\n*Foetal tissue transplantation\n*Surgery and DBS only used with people with severe PD that does not respond to drug treatment (L-dopa etc)\n*DBS with implanted electrodes results in a temporary, reversible lesion at the site of the stimulation\n*Three sites:\n**Thalamus (ventral intermediate nucleus)\n**Pallidus (globus pallidus)\n**Sub-thalamic nucleus\n*Blilateral thalamectomy no longer done because of high rate of severe cognitive deficits (memory, language, executive functions)\n*Unilateral thalamectomy results in substantial reduction or elimination of tremor, but does nothing for \n**Rigidity\n**Bradykinesia/akinesia\n**Dyskinesias that are a side effect of chronic L dopa treatment\n**As a result there is little or no effect on ADL/~QoL\n*Bilateral thalamic DBS\n**Has a much lower rate of side effects that thalamectomy\n**But like thalamectomy only has an effect on tremor\n*Pallidotomy and subthalamic nucleotomy have very similar effects\n**Unilateral surgery results in \n***Substantial reduction or elimination of tremor\n***Reduced rigidity\n***Reduced bradykinesia/akinesia\n***Reduced dyskinesias that are a side effect of chronic L dopa treatment\n***Reduced drug dosages\n**About 50% of patients report improved quality of life and improved ADL\n*Pallidus and STN\n**Bilateral DBS\n***Has a much lower rate of side effects that surgery\n***Higher rates of beneficial effects; but effects essentially the same\n***substantial reduction or elimination of tremor\n***Reduced rigidity\n***Reduced bradykinesia/akinesia\n***Reduced dyskinesias that are a side effect of chronic L dopa treatment\n***Reduced drug dosages\n**About 70% of patients report improved quality of life and improved ADL\n*No systematic comparison on GP and STN DBS\n**Both have significantly better effects than surgery at the corresponding site

*Using anticonvulsant drugs - 70-80% of people enter into prolonged remission with just a single drug\n*If blood levels are monitored, seizure control can be achieved with minimal side effects\n**Most often reported side effects are drowsiness, dullness, lack of mental agility, irritability, nausea, skin rash, lack of co-ordinaton, and, in children, hyperactivity\n*Some 20% of people with epilepsy have a chronic disorder that does not respond to a single drug\n**Only about 10% of these people respond to treatment with multiple drugs\n*[[Surgery for epilepsy]]

*Tremor at rest: best observed with eyes closed and with distraction (eg backwards counting)\n**Rest tremor is characteristic of extrapyramidal disease\n*Intention tremor: tremor increases as target is approached\n**Intention tremor is characteristic of cerebellar [[ataxia|Ataxia]]\n*Action tremor: tremor throughout movement\n*Postural tremor: ‘put your hands out and hold them’\n

*Before streptomycin (introduced c1946) this was invariably fatal\n*Now rare, except in HIV where relatively common\n!Presentation\n*Insidious (ie gradual) onset\n*General malaise\n*Headache, mild fever, vomiting, drowsiness, slight neck stiffness\n*Lapsing into coma\n!Treatment and prognosis\n*Treated with antituberculous drugs esp. streptomycin\n*In mid 1970s mortality was 30-50%\n*Now mortality c10% if treated early (and not immunosuppressed), with neurological sequelae in about 20%

*[[Incidence of cerebral tumour]]\n*[[Physiological consequence of cerebral tumour]]\n*[[Cognitive consequence of cerebral tumour]]\n*[[Tumours - grading]]\n*Types of tumour\n**[[Intrinsic cerebral tumours]]\n**[[Extrinsic cerebral tumours]]\n***[[Acoustic neuroma]]

*Grade I\n**The tumour grows slowly, has cells that look similar to normal cells, and rarely spreads into nearby tissues. It may be possible to remove the entire tumour by surgery.\n*Grade II\n**The tumour grows slowly, but may spread into nearby tissue and may become a higher-grade tumour.\n*Grade III\n**The tumour grows quickly, is likely to spread into nearby tissue, and the tumour cells look very different from normal cells.\n*Grade IV\n**The tumour grows very aggressively, has cells that look very different from normal cells, and is difficult to treat successfully. \n\n*The chance of recovery (prognosis) and choice of treatment depend on the type, grade, and location of the tumour and whether cancer cells remain after surgery and/or have spread to other parts of the brain. \n

*[[Infarction or ischaemic stroke]] 80% of strokes\n**[[Embolic Stroke]] 20% of these\n**[[Thrombotic Stroke]] 60% of these\n**[[Small Vessel Disease or Lacunar Stroke]] 20% of these\n*[[Haemorrhage]] 20% of strokes\n*[[Hypotensive or Anoxic Stroke]] rare

*Usually caused by brain stem trauma\n*Assessed typically using the [[Glasgow coma scale|GCS]]\n*Lucid intervals are not unusual (25% talk between trauma onset and deterioration into coma

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// for security reason no password as macro parameter\n var label;\n if (document.location.toString().substr(0,4) == "http")\n label = this.label.saveLabel;\n else\n label = this.label.uploadLabel;\n var prompt;\n if (storeUrl) {\n prompt = this.label.promptParamMacro.toString().format([this.toDirUrl(storeUrl, uploadDir, username)]);\n }\n else {\n prompt = this.label.promptOption;\n }\n createTiddlyButton(place, label, prompt, \n function () {\n config.macros.upload.upload(storeUrl, toFilename, uploadDir, backupDir, username, password); \n return false;}, \n null, null, this.accessKey);\n};\nconfig.macros.upload.UploadLog = function() {\n return new config.lib.Log('UploadLog', " !storeUrl | !uploadDir | !toFilename | !backupdir | !origin |" );\n};\nconfig.macros.upload.UploadLog.prototype = config.lib.Log.prototype;\nconfig.macros.upload.UploadLog.prototype.startUpload = function(storeUrl, toFilename, uploadDir, backupDir) {\n var line = " [[" + config.lib.file.basename(storeUrl) + "|" + storeUrl + "]] | ";\n line += uploadDir + " | " + toFilename + " | " + backupDir + " |";\n this.newLine(line);\n};\nconfig.macros.upload.UploadLog.prototype.endUpload = function() {\n this.addToLine(" Ok |");\n};\nconfig.macros.upload.basename = config.lib.file.basename;\nconfig.macros.upload.dirname = config.lib.file.dirname;\nconfig.macros.upload.toRootUrl = function (storeUrl, username)\n{\n return root = (this.dirname(storeUrl)?this.dirname(storeUrl):this.dirname(document.location.toString()));\n}\nconfig.macros.upload.toDirUrl = function (storeUrl, uploadDir, username)\n{\n var root = this.toRootUrl(storeUrl, username);\n if (uploadDir && uploadDir != '.')\n root = root + '/' + uploadDir;\n return root;\n}\nconfig.macros.upload.toFileUrl = function (storeUrl, toFilename, uploadDir, username)\n{\n return this.toDirUrl(storeUrl, uploadDir, username) + '/' + toFilename;\n}\nconfig.macros.upload.upload = function(storeUrl, toFilename, uploadDir, backupDir, username, password)\n{\n // parameters initialization\n storeUrl = (storeUrl ? storeUrl : config.options.txtUploadStoreUrl);\n toFilename = (toFilename ? toFilename : config.options.txtUploadFilename);\n backupDir = (backupDir ? backupDir : config.options.txtUploadBackupDir);\n uploadDir = (uploadDir ? uploadDir : config.options.txtUploadDir);\n username = (username ? username : config.options.txtUploadUserName);\n password = config.options.pasUploadPassword; // for security reason no password as macro parameter\n if (!password || password === '') {\n alert(config.macros.upload.messages.passwordEmpty);\n return;\n }\n if (storeUrl === '') {\n storeUrl = config.macros.upload.defaultStoreScript;\n }\n if (config.lib.file.dirname(storeUrl) === '') {\n storeUrl = config.lib.file.dirname(document.location.toString())+'/'+storeUrl;\n }\n if (toFilename === '') {\n toFilename = config.lib.file.basename(document.location.toString());\n }\n\n clearMessage();\n // only for forcing the message to display\n if (version.major < 2)\n store.notifyAll();\n if (!storeUrl) {\n alert(config.macros.upload.messages.urlParamMissing);\n return;\n }\n // Check that file is not locked\n if (window.BidiX && BidiX.GroupAuthoring && BidiX.GroupAuthoring.lock) {\n if (BidiX.GroupAuthoring.lock.isLocked() && !BidiX.GroupAuthoring.lock.isMyLock()) {\n alert(config.macros.upload.messages.fileLocked);\n return;\n }\n }\n \n var log = new this.UploadLog();\n log.startUpload(storeUrl, toFilename, uploadDir, backupDir);\n if (document.location.toString().substr(0,5) == "file:") {\n saveChanges();\n }\n var toDir = config.macros.upload.toDirUrl(storeUrl, toFilename, uploadDir, username);\n displayMessage(config.macros.upload.messages.aboutToUpload.format([toDir]), toDir);\n this.uploadChanges(storeUrl, toFilename, uploadDir, backupDir, username, password);\n if(config.options.chkGenerateAnRssFeed) {\n //var rssContent = convertUnicodeToUTF8(generateRss());\n var rssContent = generateRss();\n var rssPath = toFilename.substr(0,toFilename.lastIndexOf(".")) + ".xml";\n this.uploadContent(rssContent, storeUrl, rssPath, uploadDir, '', username, password, \n function (responseText) {\n if (responseText.substring(0,1) != '0') {\n displayMessage(config.macros.upload.messages.rssFileNotUploaded.format([rssPath]));\n }\n else {\n var toFileUrl = config.macros.upload.toFileUrl(storeUrl, rssPath, uploadDir, username);\n displayMessage(config.macros.upload.messages.rssFileUploaded.format(\n [toFileUrl]), toFileUrl);\n }\n // for debugging store.php uncomment last line\n //DEBUG alert(responseText);\n });\n }\n return;\n};\n\nconfig.macros.upload.uploadChanges = function(storeUrl, toFilename, uploadDir, backupDir, \n username, password) {\n var original;\n if (document.location.toString().substr(0,4) == "http") {\n original = this.download(storeUrl, toFilename, uploadDir, backupDir, username, password);\n return;\n }\n else {\n // standard way : Local file\n \n original = loadFile(getLocalPath(document.location.toString()));\n if(window.Components) {\n // it's a mozilla browser\n try {\n netscape.security.PrivilegeManager.enablePrivilege("UniversalXPConnect");\n var converter = Components.classes["@mozilla.org/intl/scriptableunicodeconverter"]\n .createInstance(Components.interfaces.nsIScriptableUnicodeConverter);\n converter.charset = "UTF-8";\n original = converter.ConvertToUnicode(original);\n }\n catch(e) {\n }\n }\n }\n //DEBUG alert(original);\n this.uploadChangesFrom(original, storeUrl, toFilename, uploadDir, backupDir, \n username, password);\n};\n\nconfig.macros.upload.uploadChangesFrom = function(original, storeUrl, toFilename, uploadDir, backupDir, \n username, password) {\n var startSaveArea = '<div id="' + 'storeArea">'; // Split up into two so that indexOf() of this source doesn't find it\n var endSaveArea = '</d' + 'iv>';\n // Locate the storeArea div's\n var posOpeningDiv = original.indexOf(startSaveArea);\n var posClosingDiv = original.lastIndexOf(endSaveArea);\n if((posOpeningDiv == -1) || (posClosingDiv == -1))\n {\n alert(config.messages.invalidFileError.format([document.location.toString()]));\n return;\n }\n var revised = original.substr(0,posOpeningDiv + startSaveArea.length) + \n allTiddlersAsHtml() + "\sn\st\st" +\n original.substr(posClosingDiv);\n var newSiteTitle;\n if(version.major < 2){\n newSiteTitle = (getElementText("siteTitle") + " - " + getElementText("siteSubtitle")).htmlEncode();\n } else {\n newSiteTitle = (wikifyPlain ("SiteTitle") + " - " + wikifyPlain ("SiteSubtitle")).htmlEncode();\n }\n\n revised = revised.replaceChunk("<title"+">","</title"+">"," " + newSiteTitle + " ");\n revised = revised.replaceChunk("<!--PRE-HEAD-START--"+">","<!--PRE-HEAD-END--"+">","\sn" + store.getTiddlerText("MarkupPreHead","") + "\sn");\n revised = revised.replaceChunk("<!--POST-HEAD-START--"+">","<!--POST-HEAD-END--"+">","\sn" + store.getTiddlerText("MarkupPostHead","") + "\sn");\n revised = revised.replaceChunk("<!--PRE-BODY-START--"+">","<!--PRE-BODY-END--"+">","\sn" + store.getTiddlerText("MarkupPreBody","") + "\sn");\n revised = revised.replaceChunk("<!--POST-BODY-START--"+">","<!--POST-BODY-END--"+">","\sn" + store.getTiddlerText("MarkupPostBody","") + "\sn");\n\n var response = this.uploadContent(revised, storeUrl, toFilename, uploadDir, backupDir, \n username, password, function (responseText) {\n if (responseText.substring(0,1) != '0') {\n alert(responseText);\n displayMessage(config.macros.upload.messages.fileNotUploaded.format([getLocalPath(document.location.toString())]));\n }\n else {\n if (uploadDir !== '') {\n toFilename = uploadDir + "/" + config.macros.upload.basename(toFilename);\n } else {\n toFilename = config.macros.upload.basename(toFilename);\n }\n var toFileUrl = config.macros.upload.toFileUrl(storeUrl, toFilename, uploadDir, username);\n if (responseText.indexOf("destfile:") > 0) {\n var destfile = responseText.substring(responseText.indexOf("destfile:")+9, \n responseText.indexOf("\sn", responseText.indexOf("destfile:")));\n toFileUrl = config.macros.upload.toRootUrl(storeUrl, username) + '/' + destfile;\n }\n else {\n toFileUrl = config.macros.upload.toFileUrl(storeUrl, toFilename, uploadDir, username);\n }\n displayMessage(config.macros.upload.messages.mainFileUploaded.format(\n [toFileUrl]), toFileUrl);\n if (backupDir && responseText.indexOf("backupfile:") > 0) {\n var backupFile = responseText.substring(responseText.indexOf("backupfile:")+11, \n responseText.indexOf("\sn", responseText.indexOf("backupfile:")));\n toBackupUrl = config.macros.upload.toRootUrl(storeUrl, username) + '/' + backupFile;\n displayMessage(config.macros.upload.messages.backupFileStored.format(\n [toBackupUrl]), toBackupUrl);\n }\n var log = new config.macros.upload.UploadLog();\n log.endUpload();\n store.setDirty(false);\n // erase local lock\n if (window.BidiX && BidiX.GroupAuthoring && BidiX.GroupAuthoring.lock) {\n BidiX.GroupAuthoring.lock.eraseLock();\n // change mtime with new mtime after upload\n var mtime = responseText.substr(responseText.indexOf("mtime:")+6);\n BidiX.GroupAuthoring.lock.mtime = mtime;\n }\n \n \n }\n // for debugging store.php uncomment last line\n //DEBUG alert(responseText);\n }\n );\n};\n\nconfig.macros.upload.uploadContent = function(content, storeUrl, toFilename, uploadDir, backupDir, \n username, password, callbackFn) {\n var boundary = "---------------------------"+"AaB03x"; \n var request;\n try {\n request = new XMLHttpRequest();\n } \n catch (e) { \n request = new ActiveXObject("Msxml2.XMLHTTP"); \n }\n if (window.netscape){\n try {\n if (document.location.toString().substr(0,4) != "http") {\n netscape.security.PrivilegeManager.enablePrivilege('UniversalBrowserRead');}\n }\n catch (e) {}\n } \n //DEBUG alert("user["+config.options.txtUploadUserName+"] password[" + config.options.pasUploadPassword + "]");\n // compose headers data\n var sheader = "";\n sheader += "--" + boundary + "\sr\snContent-disposition: form-data; name=\s"";\n sheader += config.macros.upload.formName +"\s"\sr\sn\sr\sn";\n sheader += "backupDir="+backupDir\n +";user=" + username \n +";password=" + password\n +";uploaddir=" + uploadDir;\n // add lock attributes to sheader\n if (window.BidiX && BidiX.GroupAuthoring && BidiX.GroupAuthoring.lock) {\n var l = BidiX.GroupAuthoring.lock.myLock;\n sheader += ";lockuser=" + l.user\n + ";mtime=" + l.mtime\n + ";locktime=" + l.locktime;\n }\n sheader += ";;\sr\sn"; \n sheader += "\sr\sn" + "--" + boundary + "\sr\sn";\n sheader += "Content-disposition: form-data; name=\s"userfile\s"; filename=\s""+toFilename+"\s"\sr\sn";\n sheader += "Content-Type: " + config.macros.upload.contentType + "\sr\sn";\n sheader += "Content-Length: " + content.length + "\sr\sn\sr\sn";\n // compose trailer data\n var strailer = new String();\n strailer = "\sr\sn--" + boundary + "--\sr\sn";\n //strailer = "--" + boundary + "--\sr\sn";\n var data;\n data = sheader + content + strailer;\n //request.open("POST", storeUrl, true, username, password);\n try {\n request.open("POST", storeUrl, true); \n }\n catch(e) {\n alert(config.macros.upload.messages.crossDomain + "\snError:" +e);\n exit;\n }\n request.onreadystatechange = function () {\n if (request.readyState == 4) {\n if (request.status == 200)\n callbackFn(request.responseText);\n else\n alert(config.macros.upload.messages.errorUploadingContent + "\snStatus: "+request.status.statusText);\n }\n };\n request.setRequestHeader("Content-Length",data.length);\n request.setRequestHeader("Content-Type","multipart/form-data; boundary="+boundary);\n request.send(data); \n};\n\n\nconfig.macros.upload.download = function(uploadUrl, uploadToFilename, uploadDir, uploadBackupDir, \n username, password) {\n var request;\n try {\n request = new XMLHttpRequest();\n } \n catch (e) { \n request = new ActiveXObject("Msxml2.XMLHTTP"); \n }\n try {\n if (uploadUrl.substr(0,4) == "http") {\n netscape.security.PrivilegeManager.enablePrivilege("UniversalBrowserRead");\n }\n else {\n netscape.security.PrivilegeManager.enablePrivilege("UniversalXPConnect");\n }\n } catch (e) { }\n //request.open("GET", document.location.toString(), true, username, password);\n try {\n request.open("GET", document.location.toString(), true);\n }\n catch(e) {\n alert(config.macros.upload.messages.crossDomain + "\snError:" +e);\n exit;\n }\n \n request.onreadystatechange = function () {\n if (request.readyState == 4) {\n if(request.status == 200) {\n config.macros.upload.uploadChangesFrom(request.responseText, uploadUrl, \n uploadToFilename, uploadDir, uploadBackupDir, username, password);\n }\n else\n alert(config.macros.upload.messages.errorDownloading.format(\n [document.location.toString()]) + "\snStatus: "+request.status.statusText);\n }\n };\n request.send(null);\n};\n\n//}}}\n////===\n\n////+++!![Initializations]\n\n//{{{\nconfig.lib.options.init('txtUploadStoreUrl','store.php');\nconfig.lib.options.init('txtUploadFilename','');\nconfig.lib.options.init('txtUploadDir','');\nconfig.lib.options.init('txtUploadBackupDir','');\nconfig.lib.options.init('txtUploadUserName',config.options.txtUserName);\nconfig.lib.options.init('pasUploadPassword','');\nsetStylesheet(\n ".pasOptionInput {width: 11em;}\sn"+\n ".txtOptionInput.txtUploadStoreUrl {width: 25em;}\sn"+\n ".txtOptionInput.txtUploadFilename {width: 25em;}\sn"+\n ".txtOptionInput.txtUploadDir {width: 25em;}\sn"+\n ".txtOptionInput.txtUploadBackupDir {width: 25em;}\sn"+\n "",\n "UploadOptionsStyles");\nconfig.shadowTiddlers.UploadDoc = "[[Full Documentation|http://tiddlywiki.bidix.info/l#UploadDoc ]]\sn"; \nconfig.options.chkAutoSave = false; saveOptionCookie('chkAutoSave');\n\n//}}}\n////===\n\n////+++!![Core Hijacking]\n\n//{{{\nconfig.macros.saveChanges.label_orig_UploadPlugin = config.macros.saveChanges.label;\nconfig.macros.saveChanges.label = config.macros.upload.label.saveToDisk;\n\nconfig.macros.saveChanges.handler_orig_UploadPlugin = config.macros.saveChanges.handler;\n\nconfig.macros.saveChanges.handler = function(place)\n{\n if ((!readOnly) && (document.location.toString().substr(0,4) != "http"))\n createTiddlyButton(place,this.label,this.prompt,this.onClick,null,null,this.accessKey);\n};\n\n//}}}\n////===\n

*[[Alzheimer's disease]]\n*[[Vascular dementia]]\n*[[Demetia with Lewy Bodies]]\n*[[Fronto-temporal dementia - Frontal variant]]\n*[[Fronto-temporal dementia - Temporal variant]]\n*[[Progressive aphasia]]\n**[[Progressive non-fluent aphasia]]\n**Progressive fluent aphasia = Semantic dementia = [[Fronto-temporal dementia - Temporal variant]]\n*Other rare dementias\n**[[Parkinson's disease]] (related to DLB)\n**[[Huntingdon's disease]]\n**[[CJD]]\n**[[AIDS-related dementia]]

!Prevalence, etc.\n*Approx 10-50% of people with dementia have vascular dementia\n*25-50% of stroke patients have dementia\n*Estimated to be half as frequent as AD\n!Due to\n*Multiple infarcts – Multi-infarct dementia (MID)\n*Resulting in (mostly) cortical lesions\n*Small vessel disease\n**Resulting in subcortical lesions\n*Chronic ischaemia/hypoperfusion\n![[Features of VD]]\n*Abrupt onset and stepwise fluctuating course\n*With small vessel disease and chronic hypoperfusion onset may be more insidious\n*[[Language features of VD]]\n\n

*No response to pain or other stimuli\n*No evidence of cortical responsiveness\n**Absent or very abnormal ~EEGs\n*Recovery from persistent vegetative state (>30 days) is 50-60% within 6 months, very rare after a year\n*May experience sleep/wake cycles, or be in a state of chronic wakefulness\n*May exhibit some behaviours that can be construed as arising from partial consciousness, such as\n**Grinding the teeth\n**Swallowing\n**Smiling\n**Shedding tears\n**Grunting\n**Moaning\n**Screaming

*Functions\n**Semantic processing (particularly for concrete items)\n**Mapping from semantics to phonology\n**? Visual word recognition\n*Blood supply\n**Is on the watershed between the [[MCA|Middle cerebral artery (MCA)]] and the [[PCA|Posterior cerebral artery]]\n**Therefore not often affected by [[stroke|Stroke]]\n**Often affected by [[Semantic dementia]]\n*Also referred to as the inferolateral temporal cortex

*Functions\n**Long term memory - verbal more on the left, visual more on the right\n*Bilateral lesions can cause severe amnesia

*Are typically very premature and have been in special care baby units\n*Usually used to refer to children of <1.5kg at birth\n*Many more of these children survive now\n*At 6 yrs compared with term peers very preterm children: \n**score significantly lower (approximately –1 SD) on measures of cognitive and language skills \n**have major cognitive deficits (<–2 SD) 10 to 35 times more often than the controls. \n**Deficits in speech articulation and prereading skills (<10th centile) are three to five times more frequent \n**More than 18% of very preterm children have cognitive deficits in more than five areas of functioning, compared with no control children. \n*Children who do not need hyperbaric oxygen do relatively well\n*Those that do – who typically are lighter and more premature – have a greatly increased rate of cognitive and/or linguistic delay\n*Overall VLBW children show a raised incidence of 2-4 times in developmental abnormalities

*Intracarotid sodium amytal (an anaesthetic - goes to the front 2/3 of the brain)\n*Goes initially to the ipsilateral hemisphere \n*Name pictures during presentation, and then recall\n*Verbal memory impairment is a more reliable indicator of language dominance than aphasia during testing

Hello there.\nThese are revision tiddlers for a Neurology course I've just done. Please feel free to edit if you think there are mistakes, or if you want to add cross references, tags, or new tiddlers.

*Due to lesion of [[Wernicke's area]]\n*Fluent paraphasic speech production\n*Impaired repetition\n*Poor auditory comprehension

*Probably important for word recognition / semantics / phonology

!Also known as\n*Cerebrovascular accident (CVA) - This has fallen out of use\n*Apoplexy - In the olden days\n!Key characteristcs\n*Sudden onset\n*Persistent effects (>24 hours)\n**If effects last less than 24 hours, it is called a transient ischaemic attack (TIA)\n*Of vascular origin\n!WHO definition (1989)\n*Stroke is a series of rapidly developing clinical signs of focal (or global) disturbance of cerebral function, with symptoms lasting 24 hours or longer or leading to death with no apparent cause other than of vascular origin.

*~ICD-10 definition\n**“A syndrome due to disease of the brain, usually of a chronic or progressive nature in which there is disturbance of multiple higher cortical function including memory, thinking, orientation, comprehension, calculation, learning capacity, language and judgment. Consciousness is not clouded. The impairments of cognitive function are commonly accompanied , and occasionally preceded by deterioration in emotional controls, social behaviour or motivation”\n*Becomes increasingly global\n*Affects work and social life

*Sudden physical assault on the head causing damage to the brain\n*Damage can be focal or diffuse\n*Minimum criteria - some loss of consciousness\n*Two types\n**Penetrating injury\n***Laceration of brain\n***Bone fragments - infection\n***[[Haemorrhage]]\n**Closed head injury\n***Contusion (bruising)\n***[[Coup and contracoup injuries]]\n***[[Shearing injuries to the base of the brain]]\n***[[Haemorrhage]]

*Deletion on chromosome 7\n*Facial dysmorphia\n**Puffiness around the eyes, a short nose with a broad nasal tip, wide mouth, full cheeks, full lips, and a small chin. \n**People with WS are also likely to have a long neck, sloping shoulders, short stature, limited mobility in their joints, and curvature of the spine. \n*Cardiac and renal abnormalities common\n*Learning disability\n*‘overfriendly’ personality\n*Surprisingly good language ?\n**Bellugi et al (1990) claimed\n***SLI: language <IQ\n***WS: language >IQ\n***WS particularly good at grammatical morphology – delayed onset but then develops rapidly (e.g. Rice 2003)\n**Disputed though: many studies have documented poor pragmatics, poor semantics and sometimes poor morphosyntax

*Due to an abnormality in copper metabolism \n*As a result of an autosomal recessive disorder\n*So if both parents carry the gene ¼ children will have WD\n*Rare (prevalence 3/100,000)\n*Around 1/3 present with personality change/psychiatric disorder\n*Around 2/3 present with movement disorder – either Parkinsonian or dystonic\n*Characteristic '~Kayser-Fleischer ring’ in iris due to copper accumulation\n*[[Dysarthria]] common\n*Can be treated with copper chelating agents

*A selective difficulty in spoken language comprehension\n*Comprehension of non-verbal sounds is normal\n*Almost always requires bilateral lesions to the posterior [[superior temporal gyrus|Superior and middle temporal gyri]]\n*If [[Heschl's gyrus]] is included, patients are cortically deaf

*Uses the BOLD response\n*When brain is active, blood flow increases more than is necessary\n*As a result there is less deoxyhaemoglobin and more oxyhaemoglobin in active tissue \n*There is a greater magnetic signal from deoxyhaemoglobin than oxyhaemoglobin\n*Has better temporal resolution than PET: but metabolism can take up to 2 secs to be reflected in blood flow.\n*Has better spatial resolution than PET c5mm\n*Signals are attenuated by air in sinuses - as a result poor ability to detect signal from inferior temporal regions\n

Can be 'saved' quite easily with early treatment to reduce its impact

Tiny inflammations of small arterial walls

Narrowing of the lumen