Neuro Flashcards
Causes of cerebellum injury
P - Posterior fossa tumour A - Alcohol S - Multiple sclerosis T - Trauma R - Rare causes I - Inherited (e.g. Friedreich's ataxia) E - Epilepsy treatments S - Stroke
MRC power grading
Grade 0 No muscle movement
Grade 1 Trace of contraction
Grade 2 Movement at the joint with gravity eliminated
Grade 3 Movement against gravity, but not against added resistance
Grade 4 Movement against an external resistance with reduced strength
Grade 5 Normal strength
Causes of 3rd nerve palsy
D - DM
W - Webers
N - Neuro: MS
ANd - Aneurysm (post communicating) - rule out if painful 3rd nerve palsy
O - Other: SLE, Temporal arteritis
U - Uncal herniation (false localising sign)
T - Thrombosis of cavernous sinus
Oxford stroke classification
The following criteria should be assessed:
- unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
- homonymous hemianopia
- higher cognitive dysfunction e.g. dysphasia
Total anterior circulation infarcts (TACI, c. 15%)
involves middle and anterior cerebral arteries
all 3 of the above criteria are present
Partial anterior circulation infarcts (PACI, c. 25%)
involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
2 of the above criteria are present
Lacunar infarcts (LACI, c. 25%)
involves perforating arteries around the internal capsule, thalamus and basal ganglia
presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis
Posterior circulation infarcts (POCI, c. 25%) involves vertebrobasilar arteries presents with 1 of the following: 1. cerebellar or brainstem syndromes 2. loss of consciousness 3. isolated homonymous hemianopia
Extradural vs subdural
Extradural = lucid period, usually following major head injury. Subdural = fluctuating consciousness, often following trivial injury in the elderly or alcoholics
Features wernicke’s encephalopathy
A classic triad of ophthalmoplegia/nystagmus, ataxia and confusion
nystagmus (the most common ocular sign) ophthalmoplegia ataxia confusion, altered GCS peripheral sensory neuropathy
Korsakoff’s syndrome
- amnesia
- confabulation
GCS
Eyes -4 Spontaneous To sound To pressure None
Verbal-5 Orientated Confused Words Sounds None
Motor-6 Obey commands Localising Normal flexion from pain Abnormal flexion (decorticate) Extension (decerebrate) None
Alzheimers management
Non-pharmacological management
NICE recommend offering ‘a range of activities to promote wellbeing that are tailored to the person’s preference’
NICE recommend offering group cognitive stimulation therapy for patients with mild and moderate dementia
other options to consider include group reminiscence therapy and cognitive rehabilitation
Pharmacological management
NICE updated it’s dementia guidelines in 2018
the three acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) as options for managing mild to moderate Alzheimer’s disease
memantine (an NMDA receptor antagonist) is in simple terms the ‘second-line’ treatment for Alzheimer’s, NICE recommend it is used in the following situation reserved for patients with
→ moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
→ as an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
→ monotherapy in severe Alzheimer’s
Managing non-cognitive symptoms
NICE does not recommend antidepressants for mild to moderate depression in patients with dementia
antipsychotics should only be used for patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress
Sodium valproate side effects
Valproate Appetite and weight gain Liver failure Pancreatitis Reversible hair loss Oedema Ataxia Tremor + teratogenicity + thrombocytopenia Encephalopathy
Visual defect due to lobe damage
left homonymous hemianopia means visual field defect to the left, i.e. lesion of right optic tract
homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior)
incongruous defects = optic tract lesion; congruous defects= optic radiation lesion or occipital cortex
NF2
Bilateral vestibular schwannomas
Multiple intracranial schwannomas, mengiomas and ependymomas
NF1
Café-au-lait spots (>= 6, 15 mm in diameter) Axillary/groin freckles Peripheral neurofibromas Iris hamatomas (Lisch nodules) in > 90% Scoliosis Pheochromocytomas
Intranuclear opthalmoplegia
Overview
a cause of horizontal disconjugate eye movement
due to a lesion in the medial longitudinal fasciculus, which connects the IIIrd, IVth and VIth cranial nuclei
Features
impaired adduction of the eye on the same side as the lesion
horizontal nystagmus of the abducting eye on the contralateral side
Causes
multiple sclerosis
vascular disease
Reflexes
Ankle S1-S2
Knee L3-L4
Biceps C5-C6
Triceps C7-C8
Most common complications (long term of meningitis)
deafness (most common)
other neurological: epilepsy, paralysis
infective: sepsis, intracerebral abscess
pressure: brain herniation, hydrocephalus
Most common cause Guilin barre
Campylobacter jejuni
What is Hoffman’s sign ?
is a reflex test to assess for cervical myelopathy. It is performed by gently flicking one finger on a patient’s hand. A positive test results in reflex twitching of the other fingers on the same hand in response to the flick.
Acoustic neuroma features
Vestibular schwannomas (sometimes referred to as acoustic neuromas) account for approximately 5% of intracranial tumours and 90% of cerebellopontine angle tumours.
Features can be predicted by the affected cranial nerves
cranial nerve VIII: hearing loss, vertigo, tinnitus
cranial nerve V: absent corneal reflex
cranial nerve VII: facial palsy
Bilateral acoustic neuromas are seen in neurofibromatosis type 2
MRI of the cerebellopontine angle is the investigation of choice
Mx trigeminal neuralgia
carbamazepine is first-line
failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology
Tx generalised tonic clonic
sodium valproate
second line: lamotrigine, carbamazepine
Tx absence
sodium valproate or ethosuximide
sodium valproate particularly effective if co-existent tonic-clonic seizures in primary generalised epilepsy
Tx myoclonic
sodium valproate
second line: clonazepam, lamotrigine
Tx partial
carbamazepine or lamotrigine
second line: levetiracetam, oxcarbazepine or sodium valproate
Phenytoin adverse effects and monitoring
Adverse effects
Phenytoin is associated with a large number of adverse effects. These may be divided into acute, chronic, idiosyncratic and teratogenic. Phenytoin is also an inducer of the P450 system.
Acute
initially: dizziness, diplopia, nystagmus, slurred speech, ataxia
later: confusion, seizures
Chronic
common: gingival hyperplasia (secondary to increased expression of platelet derived growth factor, PDGF), hirsutism, coarsening of facial features, drowsiness
megaloblastic anaemia (secondary to altered folate metabolism)
peripheral neuropathy
enhanced vitamin D metabolism causing osteomalacia
lymphadenopathy
dyskinesia
Idiosyncratic fever rashes, including severe reactions such as toxic epidermal necrolysis hepatitis Dupuytren's contracture* aplastic anaemia drug-induced lupus
Teratogenic
associated with cleft palate and congenital heart disease
Monitoring
Phenytoin levels do not need to be monitored routinely but trough levels, immediately before dose should be checked if:
adjustment of phenytoin dose
suspected toxicity
detection of non-adherence to the prescribed medication
Mx cluster
acute: 100% oxygen (80% response rate within 15 minutes), subcutaneous triptan (75% response rate within 15 minutes)
prophylaxis: verapamil is the drug of choice. There is also some evidence to support a tapering dose of prednisolone
NICE recommend seeking specialist advice from a neurologist if a patient develops cluster headaches with respect to neuroimaging
SAH mx
The treatment in spontaneous SAH is in accordance with the causative pathology
Most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
Until the aneurysm is treated, the patient should be kept on strict bed rest, well controlled blood pressure and should avoid straining in order to prevent a re-bleed of the aneurysm
Vasospasm is prevented using a 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature) and treated with hypervolaemia, induced-hypertension and haemodilution
Hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculo-peritoneal shunt
Risk factors idiopathic intercranial hypertension
obesity
female sex
pregnancy
drugs*: oral contraceptive pill, steroids, tetracycline, vitamin A, lithium
idiopathic intercranial hypertension Mx
weight loss
diuretics e.g. acetazolamide
topiramate is also used, and has the added benefit of causing weight loss in most patients
repeated lumbar puncture
surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
Tribe,inal neuralgia mx
carbamazepine is first-line
failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology
Trigeminal neuralgia red flags
Sensory changes
Deafness or other ear problems
History of skin or oral lesions that could spread perineurally
Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
Optic neuritis
A family history of multiple sclerosis
Age of onset before 40 years
Triptan contraindications
patients with a history of, or significant risk factors for, ischaemic heart disease or cerebrovascular disease
Triptan adverts effects
triptan sensations’ - tingling, heat, tightness (e.g. throat and chest), heaviness, pressure
Causes of Parkinsonism
Parkinson's disease drug-induced e.g. antipsychotics, metoclopramide - see below progressive supranuclear palsy multiple system atrophy Wilson's disease post-encephalitis dementia pugilistica (secondary to chronic head trauma e.g. boxing) toxins: carbon monoxide, MPTP
Drugs causing Parkinsonism
phenothiazines: e.g. chlorpromazine, prochlorperazine
butyrophenones: haloperidol, droperidol
metoclopramide
MND mx
Riluzole
prevents stimulation of glutamate receptors
used mainly in amyotrophic lateral sclerosis
prolongs life by about 3 months
Respiratory care
non-invasive ventilation (usually BIPAP) is used at night
studies have shown a survival benefit of around 7 months
Prognosis
poor: 50% of patients die within 3 years
Confirming SAH
Computed tomography (CT) head Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system. CT is negative for SAH (no blood seen) in 7% of cases. Lumbar puncture (LP) Used to confirm SAH if CT is negative. LP is performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown). Xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure) Referral to neurosurgery to be made as soon as SAH is confirmed
To SAH
Treatment
The treatment in spontaneous SAH is in accordance with the causative pathology
Most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
Until the aneurysm is treated, the patient should be kept on strict bed rest, well controlled blood pressure and should avoid straining in order to prevent a re-bleed of the aneurysm
Vasospasm is prevented using a 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature) and treated with hypervolaemia, induced-hypertension and haemodilution
Hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculo-peritoneal shunt
Acoustic neuroma
Vestibular schwannomas (sometimes referred to as acoustic neuromas) account for approximately 5% of intracranial tumours and 90% of cerebellopontine angle tumours.
Features can be predicted by the affected cranial nerves
cranial nerve VIII: hearing loss, vertigo, tinnitus
cranial nerve V: absent corneal reflex
cranial nerve VII: facial palsy
Bilateral acoustic neuromas are seen in neurofibromatosis type 2
MRI of the cerebellopontine angle is the investigation of choice
MS acute
High dose steroids (e.g. oral or IV methylprednisolone) may be given for 5 days to shorten the length of an acute relapse. It should be noted that steroids shorten the duration of a relapse and do not alter the degree of recovery (i.e. whether a patient returns to baseline function)
MS mx
Disease modifying drugs
Beta-interferon has been shown to reduce the relapse rate by up to 30%. Certain criteria have to be met before it is used:
relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided
secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)
reduces number of relapses and MRI changes, however doesn’t reduce overall disability
Other drugs used in the management of multiple sclerosis include:
glatiramer acetate: immunomodulating drug - acts as an ‘immune decoy’
natalizumab: a recombinant monoclonal antibody that antagonises Alpha-4 Beta-1-integrin found on the surface of leucocytes, thus inhibiting migration of leucocytes across the endothelium across the blood-brain barrier
fingolimod: sphingosine 1-phosphate receptor modulator, prevents lymphocytes from leaving lymph nodes. An oral formulation is available
Essential tremor mx
propranolol is first-line
primidone is sometimes used
Neuropathic pain mx
first-line treatment*: amitriptyline, duloxetine, gabapentin or pregabalin
if the first-line drug treatment does not work try one of the other 3 drugs
tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
pain management clinics may be useful in patients with resistant problems
Cerebellar signs
D - Dysdiadochokinesia, Dysmetria (past-pointing)
A - Ataxia (limb, truncal)
N - Nystamus (horizontal = ipsilateral hemisphere)
I - Intention tremour
S - Slurred staccato speech, Scanning dysarthria
H - Hypotonia
Causes of cerebellar signs
Friedreich's ataxia, ataxic telangiectasia neoplastic: cerebellar haemangioma stroke alcohol multiple sclerosis hypothyroidism drugs: phenytoin, lead poisoning paraneoplastic e.g. secondary to lung cancer
Myasthenia gravies mx
Management
long-acting anticholinesterase inhibitors e.g. pyridostigmine
immunosuppression: prednisolone initially
thymectomy
Management of myasthenic crisis
plasmapheresis
intravenous immunoglobulins
