NEURO IMPORTANT Flashcards
What are the categories of the glasgow coma score?
How are scores used after head injury?
- Eye opening (none=1, to pain =2, to speech=3, spontaneously=4)
- Verbal response (none=1, incomprehensible=2, inappropriate=3, confused=4. oriented=5)
- Motor (none=1, extensor to painful stimulus=2, flexion to painful stimulus=3, withdraws from pain=4, localised pain to stimulus=5, obeys commands=6)
CT head immediately if <13 on initial assessment or <15 at 2 hours post op
cause of foot drop/weakness in ankle dorsiflexion
peroneal nerve palsy, localised to L4-5
Facial nerve palsy sparing the forehead
CONTRALATERAL upper motor neuron lesion e.g. stroke/tumour
Facial nerve palsy not sparing any of the face
IPSILATERAL lower motor neuron e.g. parotid tumour, Bell’s palsy
Horizontal diplopia cause
Abducens palsy
CHA₂DS₂-VASc Score use + criteria
risk of stroke in patients with Atrial Fibrillation, congestive heart failure, hypertension, age (over 75=2, 65-74=1), diabetes, prior stroke/TIA, vascular disease, sex (female)
Score of 2 or more offer anticoag, score of 1 in men=anticoag
ABCD2 score use
assess patients at risk of stroke who had a suspected TIA
Quada equina syndrome diagnostic test
urgent MRI
management of acute seizure
- check airway and apply oxygen if needed
- Recovery position
- Benzodiazepam (recommended rectal diazepam)
Past medical history of cancer and new onset back pain are features highly suggestive of
metastatic cord compression
lumbar puncture needle is inserted below
L3 level, past dura mater (epidural does not go past epidural space)
Extradural haemorrhage- presentation, appearance on scan and vessels involved
loss of consciousness, lucid period, loss of consciousness. On scan= letiform, convex appearance on scan. Caused by meningeal vessels
subdural haemorrhage normally occurs in …
vessels involved
patients with dementia or alcoholics (ppl with smaller brain). Caused by bridging veins which are small so bleeding stops quickly but haematoma forms in following weeks causing a rise in ICP
subarachnoid haemorrhage presentation and cause
sudden onset headache/photophobia/thunderclap headache/reduced consciousness, caused by rupture of berry aneurysm in circle of willis
organisms which cause meningitis
meningococcus, pneumococcus
diagnosis of meningitis
lumbar puncture (usually done after CT)- CSF shows increased white blood cells, increased protein and low glucose
Symptoms meningitis
headaches, fever, neck stiffness, photophobia/phonophobia, Kernig’s sign, Bruzdinski sign
Kernig’s sign
pain + resistance on passive knee extension with hip fully flexed, used to diagnose meningitis
Brudzinski sign
Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed. Indicative of meningitis
treatment for bacterial meningitis
(1) if organism unknown
(2) menigococcal meningitis or pneumococcal meningitis
(1) Intravenous cefotaxime aged up to 50, >50 then cefotaxime and amoxicillin
(2) cefotaxime, but can also give benzylpenicillin for meningococcal instead
Meningococcal sepsis - signs + treatment
non-blanching petechial rash, cold hands and feet, fall in BP
treatment= fluid restriction, inotropes/vasopressors, aim for pressure >70mmHg and urine output >30ml/h
presentation of encephalitis
fever, headache, focal neural signs, seizures, history of travel, tremors/hallucination
treatment of encephalitis
aciclovir within 30 mins of arriving, supportive therapy + phenytoin for seizures
tetanus cause, symptoms + treatment
cause- clostridium tetani
symptoms- muscle spasms that begin in the jaw and progress to rest of body
treatment- immunisation, tetanus immune globulin, muscle relaxants and
removal + cleaning of tissue around wound
MS- basic pathology
T cells are activated by Myelin, changing the blood-brain barrier cells to allow entry of more T cells. Leads to a Type IV hypersensitivity reaction (cell mediated) –> T cells release cytokines which attract B cells and macrophages which release antibodies and attack/destroy myelin. Leads to scarring
MS symptoms
dysarthria, nystagmus, intention tremor, muscle weakness, spasms, ataxia
MS investigations
(1) MRI shows plaques- lesions disseminated through time and space
(2) VEP
(3) lumbar puncture shows high level of antibodies
MS- pharmacology
1- acute relapse- short course steroids (methylprednisolone)
2- preventing relapse:
- B-interferon : must have had 2 attacks in the last 3 years followed by a reasonable recovery. This drug helps reduce the relapse rate + reduce the occurrence of plaques on MRI but doesn’t alter long term outcome. Only used in relapsing and remitting MS
- Glatiramer acetate : a synthetic polypeptide. Given IV. Reduces number of relapses but doesn’t alter long term outcome
- Mitoxantrone : a cytotoxic antibiotic. Is experimental. May improve long term outcome when given at 3 monthly intervals
- Natalizumab : a monoclonal antibody that inhibits adhesion so reduces the number of inflammatory cells that are able to cross the blood brain barrier. Reduces relapse rate
- Baclofen : often used as symptomatic treatment. Is an antagonist of GABA receptors.
neurotransmitters involved in epilepsy
In generalized epilepsy, a hypoactivity of GABA, which exerts a presynaptic inhibitory function, and a hyperactivity of glutamate, which acts mainly as an excitotoxic, postsynaptic excitatory neurotransmitter and partly as a presynaptically inhibitory neurotransmitter, have been reported
4 types of seizure
1- focal- in one hemisphere/lobe of cortex
2- generalised seizure- involves both cortexes. Can be tonic/clonic/atonic/myclonic (short muscle twitches)/absence seizures
3- focal onset bilateral tonic-clonic- begins in a focal region and then spreads to second hemisphere, causing generalised seizure
4- status epilepticus- seizure lasts over 5 mins, is ongoing or consists of multiple seizures without returning to normal between. Usually tonic clonic- LIFE THREATENING, TREAT STATUS EPILEPTICUS WITH RECTAL DIAZEPAM/LORAZEPAM (benzos which enhance inhibitory neurotransmitter GABA)
focal seizure- presentations
seizure limited to one hemisphere/lobe of cerebral cortex. Can be with impaired awareness (loss of awareness/responsiveness) or without (small area of brain affected causing strange sensations and movements. “jacksonian march” may be present where jerking movements start in one group and spread to other groups of muscles)
treatment- generalised tonic-clonic seizures
1st line: sodium valporate
2nd line: lamotrigine, carbamazepine
treatment- absence seizures
sodium valproate or ethosuximide
treatment myoclonic seizures
sodium valproate
second line: clonazepam, lamotrigine
focal seizures- treatment
1st line: carbamazepine or lamotrigine
2nd line: levetiracetam, oxcarbazepine or sodium valproate
Epilepsy diagnosis
(1) clinical diagnosis- eyewitness account/any physical evidence of seizure
(2) determine seizure type
(3) EEG used to assist in underlying cause/classification identification
Parkinson’s triad (+ other features!)
1- resting tremor 2- cogwheel rigidity 3- Bradykinesia/hypokinesia - no weakness! -Parkinson gait- slow shuffling
microscopic presentation of parkinson’s
lewy bodies present in the substantia nigra neurons in the pars compacta section of substantia nigra
treatment of parkinson’s
- Levadopa (dopamine replacement) 1st line if motor symptoms affect quality of life- delivered with carbidopa to prevent breakdown at BBB
- If motor symptoms not affecting quality of life, dopamine agonist or MAO inhibitor (e.g. selegliene)
1- medications that can cause parkinsonism
2- other conditions that can cause parkinsonism
1- antipsychotics e.g. haloperidol; metoclopramide (dopamine antagonist anti-emetic)
2- wilson’s disease + lewy body dementia
cerebellar syndrome presentation `
loss of coordination and nystagmus
oculomotor nerve palsy presentation
ptosis, DOWN AND OUT eye, dilated + fixed pupil
trochlear nerve palsy presentation
defective downward gaze (vertical diplopia)
trigeminal nerve palsy presentation
- trigeminal neuralgia
- loss of corneal reflex (afferent)
- loss of facial sensation
- paralysis of mastication muscles
- deviation of jaw to weak side
abducens nerve palsy presentation
palsy results in defective abduction (horizontal diplopia)
glossopharyngeal nerve palsy presentation
- hypersensitive carotid sinus reflex
- loss of gag reflex (afferent)
vagus nerve palsy presentation
- uvula deviates away from site of lesion
- loss of gag reflex
accessory nerve palsy presentation
weakness turning head to contralateral side
hypoglossal nerve palsy presentation
tongue deviates towards side of lesion
ALS (MND) effect on motor neurons + presentation
UPPER AND LOWER MOTOR NEURON SIGNS - symmetrical weakness + wasting, fasciculations (LMN signs) - hyperreflexia (UMN signs) - progressive weakness of limbs - MND NEVER AFFECTS EYE MOVEMENTS -
drugs for ALS
cannot be cured but;
rituzole- sodium channel blocker slows disease progression
baclofen- GABA agonist helps reduce spasticity
propantheline- antimuscarinic, helps improve drooling
giant cell arteritis- arteries predominantly affected
an inflammatory disease of blood vessels most commonly
involving large and medium arteries of the head, predominantly
branches of the external carotid artery. Thought to be autoimmune (giant cell granulomas and fibrosis in vessel walls)
giant cell arteritis presentation for
1-temporal branch of carotid
2- opthalmic artery
1- headaches
2- blindness due to occlusion of the ophthalmic artery leading to
ischaemia of the eyes
symptoms of giant cell arteritis
unilateral headache, facial pain, visual disturbances, jaw
claudication, flu-like symptoms, polymyalgia rheumatica
investigations for giant cell arteritis + treatment
1- ESR >100
2- Biopsy shows giant cells in elastic lumina
Treatment: corticosteroids given to weaken immune system
myasthenia gravis pathology
type II hypersensitivity reaction; B cells inappropriately make antibodies against nicotinic acetylcholine receptors on the post-synaptic side of the neuromuscular junction
Myasthenia gravis symptoms
- wake up fine but PROGRESSIVELY WEAKER THROUGH THE DAY
- weakness in extraocular muscles = ptosis/diplopia
- problems with chewing/swallowing/speaking
myasthenia gravis investigations
- antibodies- Anti-AChR antibodies
- single fibre electromyography
- CT scan to eclude thymic neoplasm
Myasthenia gravis treatment
1- Acetylcholinesterase inhibitor (e.g. neostigmine or pyridostigmine) = stops
the break down of acetylcholine by inhibiting acetylcholinesterase (the
enzyme that degrades ACh) which increases the concentration of ACh at the neuromuscular junction
2- immunosupressants e.g. prednisolone (used in relapses of MG)
3- surgical removal of thymus
Guillain-Barre Syndrome- what is it?
acute inflammatory demyelinating polyneuropathy-
A rapid onset muscle weakness caused by the immune system damaging the peripheral nerves following an infection.
Guillain-Barre Syndrome symptoms
- muscle weakness BEGINNING IN HANDS AND FEET, SYMMETRICALLY ASCENDS over a few weeks after infection
- Reflexes are reduced or absent
- Pain is common in back and limbs in early stages
- possible autonomic dysfunction- in BP, heart rate (higher pulse),
sweating & arrhythmias
organisms that can trigger Guillain-Barre Syndrome
Camylobacter jejuni (most common) Cytomegalovirus Epstein-Barr virus HIV Mycoplasma Zoster
investigations for Guillan-Barre syndrome
- lumbar puncture- rise in protein (>5.5 g/L) with normal white blood cell count
- nerve conduction studies show slow nerve conduction
- if respiratory involvement, measure FVC every 4 hours
Guillain-Barre syndrome treatment
- ventilation if respiratory involvement
- IV immunoglobulin
- plasmapheresis
anterior cerebral artery stroke presentation
contralateral hemiparesis and sensory loss, lower extremity > upper
Middle cerebral artery stroke presentation
Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia
Posterior cerebral artery stroke presentation
Contralateral homonymous hemianopia with macular sparing
Visual agnosia
Homonymous quadrantanopia causes
superior: lesion of temporal lobe
inferior: lesion of parietal lobe
mnemonic = PITS (Parietal-Inferior, Temporal-Superior)
Bitemporal hemianopia causes
lesion of optic chiasm
upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma
Homonymous hemianopia causes
incongruous defects: lesion of optic tract
congruous defects: lesion of optic radiation or occipital cortex
macula sparing: lesion of occipital cortex
Basilar artery stroke presentation
‘Locked-in’ syndrome
Lacunar stroke presentation
present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia
strong association with hypertension
common sites include the basal ganglia, thalamus and internal capsule
ischaemic stroke management
1- aspirin 300mg for 2 weeks (once haemorrhagic ruled out) + statin
2- Thrombolysis with ALTEPLASE if within 4.5 hours of onset of stroke, thrombectomy within 6 hours
3- Secondary prevention: clopidogrel long term OR aspirin + dipyridamole
stroke investigations
- FAST/ROSIER scores
- non-contrast CT head
TIA presentation + relation to stroke
- resolves within 24h
- sudden dimming/loss of vision (amaurosis fugax), aphasia, dysarthria, menrtal confusion
- having TIA increases risk of stroke in future
TIA diagnosis
- imaging by MRI
- ABCD2 score for stroke risk
- carotid doppler to look for carotid atheroma/stenosis
Huntington’s presentation + pathology
- irritability, depression and incoordination
- chorea, abnormal eye movements and poor coordination
- Due to abnormal repeated sequence (CAG) on nucleotides of the Huntington gene on chromosome 4 –> results in decreased GABA, decreased ACh, increased dopamine
Treatment of huntington’s
neuroleptics- dopamine receptor antagonists (because of increased dopamine- treat chorea)
- Tetrabenazine- depletes dopamine
Migraine treatment
1- first line= oral triptan AND NSAID or paracetamol
2- if not effective, can add metoclopromide
3- propanalol for prophylaxis
cluster headaches management
- 100% oxygen for 15mins via non-rebreathable mask
- Sumatriptan at onset of headache
- Lithium and verapamil= secondary prevention
trigeminal neuralgia treatment
pharm: CARBEMAZAPINE, lamogitrine, Phenytoin, gabapentin
surgery at peripheral nerve/trigeminal nerve root
microvascular decompression- if problem is due to abnormal intracranial blood vessels
cauda equina- symptoms
- saddle anaesthesia
- decreased anal tone
- faecal/urinary incontinence
- sexual dysfunction
- back/leg pain
causes of cauda equina
normally due to herniated disc
also tumour/met
cauda equina treatment
SURGERY to remove compression
if tumour, can use radiotherapy
carpal tunnel syndrome treatment
- splinting
- local steroid injection
- decompression surgery
alzheimer’s pathology
accumulation of B-amyloid peptide results in progressive neuronal damage, neurofibrillary tangles, increasing numbers of amyloid plaques and loss of ACh
Alzheimer’s management
- Acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine and galantamine)
- NMDA antagonist
- antipsychotics
first line treatment for Parkinsons affecting quality of life
Co-cateldopa
history of crampy exertional calf pain which improves on rest
intermittent claudication –> caused by atherosclerosis of arteries in the calves. (GB syndrome would present with weakness and numbness.)
TB drug which interacts with the oral contraceptive
Rifampicin
temporal cell arteritis treatment
prednisolone
Ramsay hunt syndrome
a form of shingles affecting the facial nerve, associated with a rash on the outer ears. As the facial nerve is affected, patient presents with Bell’s palsy. Can be prevented with shingles vaccine
Charcot triad- what is it? what is it used for?
RUQ pain, fever and jaundice
ASCENDING CHOLANGITIS
optic neuritis may be a sign of
multiple sclerosis
