3a Neuro Flashcards
What is MRI with diffusion weighted imaging used for?
MRI with diffusion weighted imaging looks at the way water molecules are arranged in the brain. Very sensitive in detecting acute infarction, especially in small strokes. (Stroke ILA)
What is a key cause of strokes in young people, associated with movements of the neck?
Vertebral artery dissection.
Stroke ILA
Is an anterior, middle or posterior circulation stroke more likely to be caused by embolic disease?
Posterior circulation strokes. (ILA)
85-year-old woman, aortic valve replacement, left sided weakness, temperature, recent tooth extraction. What is the first test you need to do?
Blood cultures - Echo important but blood cultures first because guides treatment with antibiotics. (ILA)
How would you differentiate between a migraine and subarachnoid haemorrhage?
Both cause headache, photophobia and nausea. Subarachnoid haemorrhage can result in vasospasm which can produce focal neurology, but patients are usually sicker. Symptoms resolve within a few days at the most in a migraine but last longer with SAH.
(ILA)
What are three cardiovascular causes of amaurosis fugax?
Carotid artery atherosclerotic disease
Ophthalmic artery atherosclerosis
Embolism from heart
(ILA)
What is Todd’s paresis?
Todd’s paresis is temporary focal neurological deficit following an epileptic seizure.
What score would you use to assess someone’s risk of stroke after diagnosis with AF?
CHADS2 CHF Hypertension Age >75 Diabetes Previous Stroke (2 points) or CHA2DS2VASc
How do you determine whether an NG tube is safe to use in a patient?
Test the pH of the aspirate from the NG tube. If there is no aspirate or pH is >4, an X ray is needed to confirm the position.
How does migraine present?
4 - 72 hours. Moderate to severe intensity Pounding or throbbing in nature Usually unilateral Photo and phonophobia \+/- aura (visual changes eg blurring, lines) Nausea and vomiting
Hemiplegia migraine: + hemiplegia, ataxia, changes in consciousness (stroke mimic)
Stages:
- Prodromal <3 days
- Aura <60 mins
- Headache 4-72 hrs
- Resolution - vomiting, sleeping, fading
- Postdromal/recovery phase.
[ztf]
What are the red flags to ask about in headache patients?
Fever, photophobia, neck stiffness - meningitis/encephalities
New focal neurology - haemorrhage, malignancy, stroke
Dizziness - stroke
Visual disturbance - temporal arteritis, glaucoma
Sudden onset occipital - SAH
Worse on coughing/straining/lying/bending - ICP
Severe enough to wake patient from sleep
Vomiting - ICP or CO poisining
Trauma - ICP
Pregnancy - pre-eclampsia.
[ztf]
Give the criteria for diagnosis of migraine without aura.
5 or more attacks with the following: 4-72 hours Unilateral/pulsating pain/ aggravated by activity Nausea/vomiting Photo and phonophobia
Give the criteria for diagnosis of migraine with aura.
> =2 attacks with >=1 fully reversible aura symptom: visual, sensory, speech/language, or motor weakness.
And at least 2 of the following:
At least 1 aura symptom spreads gradually over 5 mins, or at least 2 symptoms occur in succession
Each individual aura symptom lasts 5-60 mins
At least 1 aura symptom is unilateral
Followed within 60 mins by a headache
Give 3 triggers for migraine.
CHOCOLATE Chocolate Hangovers Orgasms (sexual activity) Cheese + other strong smells Oral contraceptive Lie ins Alcohol Trauma eg head injury, stress Exercise
How is migraine managed?
Will go away eventually, dark quiet room sleep.
Acute:
Triptans (5HT receptor agonists. eg sumatriptan 50mg)
NSAID/paracetamol
Anti-emetic eg metoclopramide
Prophylaxis: Topiramate (TERATOGENIC - cleft palate) propanolol amitriptyline acupuncture (recommended by NICE) If menstruation-associated, NSAIDs eg mefanamic acid around that time can help prevent.
What can cause mild ache across the forehead like a tight band?
Tension headaches.
Come on and resolve gradually, no visual changes, common.
Due to stress, depression, alcohol, skipping meals or dehydration. Muscles of frontalis, temporalis and occipitalis. No visual changes.
Describe the diagnostic criteria for infrequent episodic tension headache.
Probable: Missing one feature of tension headache diagnosis, does not fit a diagnosis of another headache disorder.
Infrequent episodic: <1 day/month
Frequent episodic: 1-14 days/ month, >3 months
Chronic: >15 days/ month, >3 months
A. >=2 of:
-bilateral
-pressing/tightening pain
-mild to moderate intensity
-not aggravated by routine physical activity.
B. No nausea or vomiting, no more than one of photo or phonophobia.
How is tension headache treated?
Reassure
Analgesia - NSAIDS (eg aspirin, ibuprofen, diclofenac)
Relaxation
Hot towel to local area
Describe the classifications of cluster headaches
Episodic: >2 cluster periods lasting 7 days to 1 year, pain free for at least 1 month at a time
Chronic: Cluster period for more than 1 year, no remission or remission less than 1 month.
Give 3 features of a headache that would suggest it is a cluster headache.
Lasts 15-180 mins
Severe, unilateral periorbital pain
Ipsilateral cranial autonomic features: Miosis, ptosis, rhinorrhoea, redness, lacrimation
Suggest a treatment for cluster headaches.
Acute attack: Subcutaneous sumatriptan, nasal spray zolmitriptan
Prophylactic verapamil, lithium, corticosteroids.
Give 3 features of a headache that would suggest temporal arteritis.
Jaw claudication
Amaurosis fugax (temporary blindness, usually in one eye)
Temporal artery and scalp tenderness
Malaise
Palpable, tender temporal arteries with reduced pulsation
How is temporal arteritis diagnosed?
Temporal artery biopsy
Blood tests:
ANCA negative, ESR >50, CRP and ALP raised, Hb lowered.
How is temporal arteritis treated?
Refer for specialist review, in the meantime:
High dose oral prednisolone (40mg) and low dose aspirin (75mg) plus a PPI for gastroprotection.
Give 3 symptoms of a carotid territory stroke.
Weakness of leg, face, arm Amaurosis fugax Impaired language Easier to spot - FAST campaign [3a lecture]
Give 3 symptoms of a posterior circulation stroke.
Dysarthria Dysphagia Diplopia Dizziness Ataxia Diplegia (symmetrical weakness) These symptoms are less obvious than carotid territory stroke symptoms, and can be more devastating.
Which is the most common type of stroke?
Ischaemic (85%)
What would you be looking for in a CT scan if you suspect stroke?
Ischemic - loss of sulci and grey matter differentiation
Haemorrhagic - blood, showing up white.
What is the Oxford stroke classification?
(=Bamford). Clinical classification of patterns of neurological deficit in acute ISCHEMIC stroke: 1. Anterior - partial or total 2. Posterior 3. Lacunar
Give 3 symptoms of anterior circulation stroke.
Contralateral weakness, sensory loss, inattention
Dysarthria
Dysphasia - receptive and expressive
Homonymous hemianopia/ visual inattention
Higher cortical dysfunction
Give 3 features specific to parietal lobe seizures.
Numbness
Tingling
Pins and needles
(The parietal lobe is responsible for orientation, pain, touch, and visual perception). PTS
Give 3 features of frontal lobe seizures.
Motor weakness
Dysphasia
Rapid recovery. PTS/ILA
Give 3 features of temporal lobe seizures.
Deja vu Dysphasia Automatisms (being unaware of actions) Fear Derealisation Olfactory/gustatory hallucinations Post-ictal confusion
What symptoms would you get if there is a problem with the occipital lobe?
Visual disturbance/ hallucination
If a patient presents with ataxia and nystagmus in the left eye, where is the lesion?
Left cerebellum.
What is a seizure?
Transient excessive hypersynchronous neuronal changes in the brain.
What is epilepsy?
A recurrent tendency towards seizures: either 2 unprovoked seizures, or 1 seizure and EEG evidence of a tendency towards seizures.
Where in the brain are complex partial seizures most likely to occur?
Temporal lobe.
Give 3 differences between a simple and complex partial seizure.
Simple - awareness unimpaired, no post-ictal symptoms, focal motor, sensory or autonomic symptoms.
Complex: Awareness impaired, may have aura or impaired awareness at onset, post-ictal confusion.
What is an absence seizure? How is it differentiated from a ‘vacant spell’?
A brief (<10 second) pause in consciousness accompanied by a 3 Hz spike and wave on ECG. Generally occur in childhood, someone stops speaking for a few seconds then continues.
When/why is an ECG useful for someone who has had a blackout?
To check for conditions that give rise to transient tachyarrhythmias, which can cause sudden death in young people, and have an abnormal ECG between events. [3a blackouts lecture]
Define a tonic-clonic seizure.
Loss of consciousness, limbs stiffen (tonic) then jerk (clonic). Can have only tonic or clonic phase. There is also post-ictal confusion and drowsiness. [ohcm]
Define a myoclonic seizure.
Sudden jerk of a limb, face or trunk; patient could be thrown violently to the ground or have a violently disobedient limb.
Define an atonic seizure.
Sudden loss of muscle tone causing a fall without LOC.
Define idiopathic generalised epilepsy (IGE).
A group of epileptic attack disorders with a strong genetic basis and often no structural brain abnormalities. They consist of typical absences, myoclonic jerks, and generalized tonic-clonic seizures, alone or in varying combinations and severity. [ILA]
How would you recognise and treat status epilepticus?
Seizure lasting >30mins but treat as status after 5 mins.
ABCDE, IV lorazepam, ECG, fluids (normal saline)
Note the time
How is non-epileptic attack disorder diagnosed?
Symptoms: Uncontrollable symptoms, one part of body, post-ictal emotion. Psychological basis. Exclude learning disability. Normal CNS exam, ECG, MRI and CT. Can co-exist with epilepsy.
What is narcolepsy?
Narcolepsy is a disorder in which sleep phenomena affect the waking state, due to a lack of orexin A and B, neuropeptides which maintain wakefulness.
What are the symptoms of narcolepsy?
People with narcolepsy usually have a few but not all of these symptoms:
Cataplexy, sleep paralysis, hypnogogic hallucinations, daytime sleepiness.
Define daytime sleepiness as a symptom.
Falling asleep with little warning in a situation that may be inappropriate.
Define hypnogogic hallucinations.
Vivid, often frightening visual, auditory or tactile hallucinations that occur as someone is falling asleep, probably caused by the overlap between wakefulness and REM sleep.
Define sleep paralysis and why it occurs.
The inability to move after waking or before falling asleep. Voluntary muscles are paralysed during sleep, but if this paralysis continues after consciousness is regained or semi-regained, a person may feel paralysed, frightened, suffocated or experience hallucinations.
Define cataplexy and why it occurs.
Cataplexy is transient muscle weakness triggered by a strong emotion, often happiness, without LOC. It usually resolves in minutes. It can be partial (face, neck, knees) or severe, causing totally body paralysis/weakness/collapse.
What is shingles?
Shingles is a condition in which a painful rash in one unilateral dermatome, malaise and fever are caused by reactivation of the varicella zoster virus.
How does shingles present?
Shingles presents as pain in a dermatomal distribution, followed by a few days of malaise and fever.
Explain the pathology of shingles.
Shingles is a reactivation of varicella zoster virus. This first infects the respiratory epithelial cells before moving to the lymph nodes in a primary infection. Secondary infection occurs when the virus travels to the liver and spleen, where it infects T cells and then keratinocytes. It travels retrogradely through sensory neurones to the dorsal root and trigeminal nerve ganglia, where it lays dormant. Reactivation may be caused by immunocompromise. When this occurs, the virus travels anterogradely to the skin, causing shingles.
How is shingles diagnosed?
Shingles is diagnosed by the way the rash looks. A Tzanck test may be used to look for multinucleated giant cells in the fluid of the vesicles, a blood test for varicella antibodies, and PCR for viral DNA.
How is shingles treated?
Treat acute zoster with antivirals: aciclovir or famciclovir. If conjunctiva affected, give acyclovir ointment.
What is Wernicke-Korsakoff syndrome?
A spectrum of disorders in which thiamine deficiency causes neuronal degeneration, producing an acute phase called Wernicke encephalopathy, and a chronic phase called Korsakoff psychosis/syndrome. It is seen most commonly in heavy drinkers.
What are the functions of thiamine in the body?
When thiamine is converted to thiamine pyrophosphate, the metabolically active form, it has multiple functions:
- Assists enzymes allowing glucose metabolism
- Help metabolise lipids and carbohydrates in the brain
- Maintains normal amino acid and neurotransmitter levels
- Assists with propagation of impulses along axons
Give 3 ways alcohol abuse causes impaired glucose metabolism.
- Alcohol abuse leads to decreased nutritional intake as alcohol is high calorie, low nutrition. Therefore thiamine deficiency occurs.
- Alcohol inhibits phosphorylation of thiamine to its metabolically active form thiamine pyrophosphate.
- Alcohol prevents absorption of thiamine by decreasing gene expression for thiamine transporter 1.
- Chronic alcohol use leads to cirrhosis, leading to impaired storage of thiamine in the liver.
Therefore thiamine is not able to assist with glucose metabolism.
Explain how thiamine deficiency causes neurological symptoms.
Thiamine is not longer able to assist with glucose metabolism, lipid and carbohydrate metabolism in the brain, propagation of neural impulses, and maintenance of amino acid and neurotransmitter levels.
The brain is particularly vulnerable to impaired glucose. This leads to haemorrhage and necrosis in the mamillary bodies, causing confusion; in the cerebellum, causing ataxia, and in the 6th cranial nerve, causing ophthalmoplegia (paralysis of lateral gaze).
What is the clinical triad of Wernicke’s encephalopathy?
Ophthalmoplegia
Ataxia
Confusion
How does Korsakoff syndrome present?
Limbic involvement -> Anterograde and retrograde amnesia
Confabulation
How is Wernicke’s encephalopathy treated?
Medical emergency - treat asap to reduce risk of Korsakoff syndrome. Thiamine infusion (IV pabrinex) over a few days.
Add glucose when thiamine is normalised - if it is added before there is enough thiamine pyrophosphate, the glucose will turn to lactic acid and there is a risk of acidosis.
What investigations would you do if someone presented with ophthalmoplegia, ataxia and confusion?
Wernicke’s encephalopathy is generally diagnosed by clinical impression but can also do:
LFT
Thiamine level blood test
MRI shows degeneration of mammillary bodies.
What is Huntington disease?
A rare neurodegenerative disease in which a repeated sequence of DNA causes an abnormal protein, leading to abnormal movements and cognitive problems.
How is Huntington disease passed on?
It is autosomal dominant. There is a 50% chance that an affected person will have an affected child. It displayed anticipation: successive generations have more CAG repeats in the gene, resulting in earlier age of onset and increased severity of the disease.
Explain the pathology of Huntington disease.
When there are more than 36 repeats of the CAG sequence, glutamine (CAG) aggregates in the putamen and caudate nuclei of the basal ganglia causing neuronal cell death and tissue loss. These areas are involved in the inhibition of movement, so the damage causes movement problems.
What is athetosis?
Athetosis, one of the symptoms of Huntington disease, is the name for slow, snake-like movements of the hands.
Give 3 symptoms of Huntington disease other than chorea.
Psychological problems: Dementia, personality changes, Depression (suicide). Abnormal eye movements Loss of co-ordination Dysarthria and dysphagia Respiratory disease eg pneumonia.
What is anticipation in terms of genetics?
Anticipation describes why symptom onset of Huntington disease is earlier with each generation. The child can inherit more repeats than the parent because there is more opportunity for repeat expansion of the CAG sequence.
What is the treatment for Huntington disease?
Only the chorea cause by increased dopamine can be treated, not the underlying disease.
Dopamine receptor antagonists eg olanzapine
Tetrabenazine - depletes dopamine.
MDT essential and core of treatment. Do not continue unnecessary medication - SEs vs benefits.
What are the cardinal features of parkinsons disease?
Resting tremor
Bradykinesia
Rigidity
[OCHM]
Explain the pathophysiology of Parkinson’s disease.
Loss of dopaminergic neurons in the substantia nigra, part of the basal ganglia which help with initiation and control of movement. Lewy bodies.
Give 3 non-motor symptoms of parkinson’s disease.
Autonomic dysfunction (postural hypotension, constipation, urinary frequency/ urgency, dribbling of saliva)
Sleep disturbance
Reduced sense of smell
What are Parkinson’s plus syndromes?
Syndromes which give rise to parkinsonian features, eg:
Progressive supranuclear palsy (PSP)
Multiple system atrophy (MSA) - autonomic and cerebellar dysfunction
Corticobasal degeneration
Lewy body dementia (LBD) - progressive cognitive decline, hallucinations, REM sleep disorders/fluctuating consciousness.
What are the risks associated with sudden withdrawal of parkinsons medications?
Acute akinesia, neuroleptic malignant syndrome.
Malabsorption can have this effect, eg abdo surgery, gastroenteritis.
Describe the first-line pharmacological treatment for parkinson’s disease and how it works.
Co-benyldopa/co-careldopa: Contains
Levodopa (dopamine precursor, which can cross the blood brain barrier, and is converted to dopamine in the brain by dopa-decarboxylase) plus carbidopa/benserazide (reduces conversion of levodopa to dopamine outside the CNS so there is more available to enter the brain).
COMT inhibitors eg entacapone slows breakdown of levodopa in the brain to extend its duration.
What is Alzheimer’s disease?
Alzheimer’s disease is a chronic neurodegenerative disease which is the most common cause of dementia in the UK.
Describe the presentation of Alzheimer’s disease. How does it differ from other types of dementia?
1.Enduring, progressive and global cognitive impairment. Visuo-spatial skill, memory, verbal ability and executive function are impaired. (other dementias affect specific domains. )
2. Anosognosia: lack of insight into the problems caused by the disease.
3. Later features: irritability, mood disturbance, behavioural change, psychosis, agnosia.
4. Cognitive impairment is progressive but non-cognitive symptoms may come and go over months.
5. Often become sedentary and uninterested towards the end.
[ohcm]
Explain the pathology of Alzheimer’s disease.
- Environmental and genetic factors play a role.
- Amyloid precursor protein (APP) is degraded to beta amyloid peptide.
- This results in progressive neuronal damage, neurofibrillary tangles, amyloid plaques, and loss of acetylcholine.
- Defective clearance of beta-amyloid plaques by macrophages due to altered macrophage gene expression.
- Neuronal loss mostly in the hippocampus, amygdala, temporal neocortex and subcortical nuclei.
- Vascular damage occurs, 95% of AD patients show vascular dementia.
[ohcm]
Give 3 risk factors for Alzheimer’s disease.
1st degree relative with AD Down's syndrome because APP is coded for on chromosome 21, of which people with Down's have an extra. APOE E4 allele homozygosity Vascular RFs: HTN, diabetes, etc Depression, loneliness (not just living alone) Low physical/cognitive activity Smoking Excessive alcohol consumption [ohcm]
What are some acetylcholinesterase inhibitors and what are the side-effects?
Donezepil, rivastigmine, galantamine.
Used for Alzheimer’s disease, increase the amount of acetylcholine in the synaptic cleft.
Cholinergic effects: vasodilation, constriction of the pupils, increased secretion of sweat, saliva and tears, bradycardia, mucus secretion in the respiratory tract,
constriction of the airways.
Explain the pathology of vascular dementia.
Cognitive decline due to cerebrovascular disease. This could be a major stroke, multiple small unrecognised strokes (multi-infarct) or chronic changes in smaller vessels (subcortical). Risk factors are any vascular ones: HTN, strokes, focal CNS signs.
How does vascular dementia present and how is this different to other dementias?
There is a sudden onset, stepwise deterioration in cognitive function, whereas other types of dementia progress more gradually. This can make it hard to recognise.
How is vascular dementia managed?
There are no approved drugs to treat VD yet. Cognitive stimulation programmes, multisensory stimulation and art/music therapy are beneficial, as well as the general support for all dementia, eg planning ahead, care co-ordination and practical help around the home.
Give five causes of dementia which can be improved.
Thiamine deficiency (eg alcohol) Syphilis Tumours (meningioma) Thyroxine/ b12 deficiency Subdural haematoma Parkinsons disease HIV (+/- cryptococcosis) Normal pressure hydrocephalus Whipple's disease Pellagra
Why would you do a physical examination in someone who presents with memory loss over years?
?Physical cause of cognitive impairment
?Parkinson’s disease
RFs eg for vascular dementia
What is hydrocephalus?
Hydrocephalus is the buildup of fluid in the brain which could lead to increased intracranial pressure. The cause varies. Presents as acute confusional state.
What investigations would you do if you suspect hydrocephalus in someone with acute confusional state?
CT head: Enlarged oval 3rd ventricle (normally slit-like), Temporal horns visible (normally not)
Send CSF for analysis
[caroll teaching]
What is normal pressure hydrocephalus?
A syndrome in which there is dilatation of the cerebral ventricles (esp 3rd) and normal CSF pressure at LP.
How does normal pressure hydrocephalus present?
Triad: Dementia, Gait ataxia, Urinary incontinence.
Progressive slowing of cognitive and motor function consistent with a pattern of subcortical dementia. Urinary incontinence is a late symptom.
What causes normal pressure hydrocephalus?
50% idiopathic
50% secondary to mechanical obstruction of CSF movement across the meninges, eg meningitis, SAH, trauma, radiotherapy.
Why does NPH cause ataxia?
It is caused by pyramidal upper motor neurone paparesis.
How is NPH diagnosed?
CT head scan: increased size of lateral ventricles, cortical thinning.
24 hour ICP monitoring: typical beta pattern.
How is hydrocephalus managed?
CSF diversion by:
- Extraventricular drain
- intracranial CSF shunt, usually ventriculo-peritoneal
- Endoscopic third ventriculostomy temporarily if concern about risk of infection with VP shunt.
Give 3 risk factors for hydrocephalus.
Anything causing obstruction of CSF travelling across the meninges:
Bacterial meningitis (pus)
Subarachnoid/intraventricular haemorrhage (blood)
Posterior fossa tumour
Spina bifida
[Carol teaching]
Why/when is important to use head imaging before an LP?
Eg if the LP is for suspected bacterial meningitis, this is a risk factor for hydrocephalus; if hydrocephalus present, LP can cause herniation. If there is an intracranial mass, LP is also contraindicated,
Describe the presentation of a right frontal lobe syndrome.
Contralateral so left side limb weakness
Motor dysphasia for dominant lobe (Broca’s area is the most inferior part of the motor strip).
(personality duplicated so only affected in bilateral disease).
[Caroll]
Describe the presentation of a left parietal lobe syndrome.
For non-dominant lobe, contralateral so right side sensory disturbance (no limb pain).
For dominant lobe, also higher sensory processing issues: dyslexia, dyscalculia, dysgraphia, astereognosis.
Describe the presentation of a dominant temporal lobe syndrome.
Dominant lobe: understanding of speech (superior temporal gyrus) and memory
No clin syndrome for non-dominant lobe
