Neurology Flashcards
What is a TIA?
Transient ishcaemia with no infarct and no permanent neurological deficit. Lasts upto 24 hours, generally less than
What are further complication risks with TIA?
2% risk of stroke in 2months if treated within 72hrs.
How do you treat TIA?
Treat with clopidogrel 75mg/d, treat BP and lipids, modify SNAP and consider endarterectomy
What is a stroke?
If acute neurologic deficits persist beyond 24 hours or are interrupted by death within that timeframe.
How common is an ischaemic stroke and what are the causes?
87% - loss of focal reigon of the brain
- Primary embolic - occlusion or critical stenosis. (carotid or cardiac in origin, artificial valves, CABG surg, DVT,, VSD, fat emboli, cncerm septic emboli (infective endocarditis)
- Systemic hypoperfusion - shock or rapid lowering of BP - watershed areas are vulnerable
- Central venous thrombosis
What is haemorrhagic transformation of stroke?
Bleeding into area of ischaemia - can occur in first few days of untreated stroke, often in first 24 hours in embolic stroke treated with coags
Risk factors for Cerebrovascular disease?
HTN (PmHx (TIA, CVD, PVD), DM, Smoking, obesity, HRT, Lipidaemia, Cancer, Old age, Male, Arrhythmia (AF)
10-25% of ischaemic strokes due to arrhythmia
What is the pathophysiology for Cerebrovascular disease?
Disease of blood vessels supplying the brain, with HTN as the most important cause – endothelial damage → collagen exposure → sustained prethrombotic state of carotid vessels → carotid atherosclerosis and stenosis. These vessels are now more sensitive to changes in BP – strokes when BP changes – ie waking up, excitation
Common site for carotid plaques?
Common/internal carotids – often at carotid bifurcation, Circle of Willis. Progressive atherosclerotic luminal stenosi
What does basal ganglia stroke present with? (what arteries are affected)
ICA → MCA → internal capsule, lenticulostriate arteries. These supply internal capsule white matter corticospinal efferents. Contralateral hemiparesis.
What is the ishcaemic cascade with hypoxia?
Excess glutamate released from tissue, lactic acid buildup, ↑apoptosis, oxygen free radicals released. Brain particularly vulnerable as it is completely reliant on aerobic metabolism.
What is the FAST acronym for patients having a stroke?
F = Facial weakness (droop), A = Arm weakness (drift), S = Speech difficulty (slur), and T = Time to act (priority of intervention)
3 cardinal features of Stroke/TIA?
Sudden onset facial weakness, Arm drift, abnormal speech - aphasia/slurring
What is amaurosis fugax?
(TIA sign: dimming) –> transient loss of vision. Embolic obstruction of centrinal retinal artery.
Vital to treat carotid artery disease!
LOC + N/V + Headache - more likely to be haemorrhagic or ischaemic?
Haemorrhagic!
Which artery is affected?
- Legs affected (contralateral lower limb), gait apraxia, personality changes (frontal lobe)
Anterior Cerebral artery!
Which artery is affected?
- Contralateral arms, face and eyes. Dysphasia if affected side is the dominant hemisphere!
Middle cerebral artery!
Which artery is affected?
- Eyes, vision loss
P (posterior) CA
Which artery is affected?
4S: Spinal nucleus of CNV, Spinothlamic, spinocerebellar, sympahetic (Horner’s)
Laterally medullary syndrome: PICA!
Which artery is affected?
4M’s: Ipslateral Tongue weakness, contralateral hemiplegia(medullary pyramid), Loss of discriminative touch - proprioception, vibration (Medial Laminiscus)
Anterior Spinal artery - Medial Medullary syndrome
What are the 4M’s:
- Motor pathway (corticospinal tract - contralateral weakness of arm and legs)
- Medial Meniscus - Contralateral loss of vibration and proprioception in the arm and leg
- Medial Longitudinal fasciculus -ipsilateral inter-nuclear ophthalmoplegia
(failure of adduction of the ipsilateral eye towards the nose and nystagmus in the opposite eye as it looks laterally) - Motor nucleus and nerve:
ipsilateral loss of the cranial nerve that is affected (3, 4, 6 or 12)
Anterior Spinal artery
The 4’s (side structures):
- Spinothalamic pathway - contralateral alteration of pain and temperature affecting the arm, leg and rarely the trunk
- Spinocerebellar pathway - ipslateral ataxia of the arm and leg
3.Sensory nucleus of the 5th cranial nerve -ipsilateral alteration of pain and temperature on the face in the distribution
of the 5th cranial nerve - Sympathetic pathway:
ipsilateral Horner’s syndrome, that is partial ptosis and a small pupil (miosis)
What happens if damage to CN 9 - Glossopharyngeal nerve
Ipslateral loss of pharnygeal sensation
What would happen if damage to vagus nerve?
Ipslateral palatal weakness
What happens if damage to Spinal accessory nerve (CN 11)?
ipsilateral weakness of the trapezius and stemocleidomastoid muscles
What happens if damage to Hypoglossal nerve?
ipsilateral weakness of the tongue
What happens if damage to the Trigeminal nerve?
Ipsilateral alteration of SENSATIONS - pain, temperature and light touch on the face back as far as the anterior two-thirds of the scalp and sparing the angle of the jaw.
What happens if damage to the Abducent nerve?
Ipsilateral weakness of abduction (lateral movement) of the eye (lateral rectus)
What happens if damage to Facial nerve (CN VII)?
Ipslateral facial weakness
Are CN I and CNII in the midbrain?
NO.
T or F?:
Is the order: Medulla, Midbrain, Pons?
No! Brainstem = Midbrain, Pons, medulla
Palsy of trochlear nerve?
eye unable to look down when the eye is looking in towards the nose (superior oblique)
What happens if damage/occlusion to the Basilar artery?
Locked in syndrome - full awareness but can only move eyes
Signs of MCA stroke?
Supples most of the lateral surface of the hemisphere,
supplies Broca’s and Wernicke’s area, deep branches supply basal ganglia and the internal capsule.
Contralateral hemiparesis Contralateral hemianaesthesia Contralateral homonymous hemianopia Gaze preference to ipsilateral side Dominant hemisphere: global aphasia May have nominal aphasia, Broca’s, Wernicke’s
Differential Diagnosis for Stroke?
Hypoglycaemia coma (check BSL), CNS lymphoma (or tumour), Head injury, Abscess, ?SDH, Drug overdose, herpes encephalitis, seizure + post-ictal deficits, venous sinus thrombosis
Ix for Stroke like symptoms?
FBE, CRP, UEC, Lipids,, BSL - Hypo?, Tox screen -alco/drugs, Neuro exam, Head non-contrast CT
What is the importance of non-contrast CT in stroke/TIA?
What will acute CT show if ischaemic stroke?
Head non-contrast CT urgently if can treat (thrombolyse) or potential haemorrhage which needs evacuation, otherwise
within 24h. CT won’t show 40% within 3-6h, will show all in 24h.
–> However will show haemorrhage, so if no haemorrhage, midline shift, or tumour → yes,
thrombolyse
To detect source of emboli?
- carotid doppler - >70% stenosis is significant
- ECG - AF?
- Thrombophilia screen if no identifiable cause
- Check for AF post-stroke - if AF suitable for cardioversion?
Pharmacological Mx of stroke?
- Prevention in AF patient with CHADSVASC of 1 warfarin, apixaban
Acute:
- NBM
- If decided not haemorrhage and >3hrs, aspirin 300mg
- If within last 3hrs, and imaging shows non-haemorrhagic stroke - alteplase (TPA) - can cause haemorrhage though. Continue with aspirin 24hrs later -300mg daily and supportive care (swallowing assessment, rehab support)
- If haemorrhagic may require neurosurg consult
thrombolysis with tPA if
3
Post stroke therapy:
1. If ischaemic - lifelong clopidogrel monotherapy. If due to non-valvular AF - cardiovert or warfarin or Aspirin with dipyridamole 2. Ace-i 3. Statin 4. ?carotid endarectomy
When do you correct carotid stenosis?
Either when symptomatic or after 70%.
What is involved in stroke rehabilitation?
– admit to stroke unit – speech/language, swallowing, physical therapy, OT, prevent pressure sores, hydrotherapy – help sufferer adapt to everyday life and maximize ADL capacity
What is the definition of Epilepsy?
Chronic neurological condition characterised by 2 or more recurrent, unprovoked seizures by an excessive disorderly discharge of cortical nerve cells. Episodic abnormal electrical activity in the brain.
Risk factors for Epilepsy/Seizures?
Acquired brain damage (trauma, stroke, brain lesion, substance abuse, substance withdrawal). family Hx, genetics, Electrolytes distrubances
_______ lobe most commonly affected by focal/partial seizures
Temporal
Difference between simple and complex seizure:
Simple - consciousness/awareness unaffected
What are the features of an absence seizure?
Decreased consciousness, no motor disturbances for about 20 seconds. No aura/postictal state. Automisms
What type of seizures are automisms related to (lip smacking, eye lid blinking)
Absence
brief jerks of the body, resulting in falls –
Myoclonic epilepsy
Differential diagnosis for seizure?
Epilepsy, Febrile convulsions, Hypoglycaemic seizure, Vasovagal episode (clear trigger and no post-ictal state), stroke, pscyhogenic non-epileptic syndrome
Medications function to ________________ and are chosen based on the epileptic syndrome of the patient.
Medications function to increase the seizure threshold, and are chosen based on the epileptic syndrome of the patient.
First line for partial seizure?
Carbamazepine
First line for absent seizure?
Ethosuximide/Valproate
First line for Tonic Clonic seizures?
Valproate
Which drug is a neuronal T-type Calcium channel blocker?
Ethosuximide
Which anti-epileptic drugs are involved in decreasing cell excitation
Phenytoin, Carbamazepine, Latotrigine, Ethosuximide
Which anti-epileptic drugs are used to increase GABA inhibition?
Benzo, Barbiturates, Vigabatrin, Valproate
What drugs act as CYP450 inducers and reduce the efficacy of COCP by increasing the metabolism of oestrogens in the pill in the liver?
Phenytoin, Carbamazepine, Phenobarbitone
Acute management of stroke?
- Call ambo
- Stabilise patient - resusc
- Take BSL - if cannot giev dextrose with thiamine
- Give O2 and take EG
- Treat with IV lorazepam or diazepam → valproate /phenytoin. If neither of these work, phenobarbital (GABA agonist - barbiturate induced coma
Restrict driving
What can happen if dextrose load is given alone in an alcoholic man?
Without thiamine - it can precipitate Wernicke-Korsakoff syndrome.
Common side effects of Clonazepam?
Behavioural chnages and excess salivary and bronchial secretions
Where is midazolam excreted?
The kidneys!
Does Clozapine cause agranulocytosis?
Yes
Which antibiotics inhibit Carbamazepine metabolism?
Erythromycin and Clarithromycin - they can lead to carbamazapine toxicity
Side effects of Carbamazepine?
Sedation, CYP450 inducer, headache, diplopia, headache, nausea.
Can lead to reversible leukopenia
at high concentrations has an ADH like action - but the resulting hyponaetremia is usually mild and asymptomatic.
Can lead to steven johnson syndrome
is Sodium valproate a CYP450 inducer or inhibitor?
Inhibitor!
How does Gabapentin act?
Inhibiting Glutamate synthesis and hence increasing brain GABA levels
How does Phenytoin work?
Blocks voltage dependent sodium channels - limiting the propagation of seizure discharges. It is high bound to albumin
What are adverse effects of phenytoin?
Neurotoxic symptoms (drowsiness, dysarthria, tremor, ataxia, diplopia, cognitive difficulties), a lupus like syndrome, Stevens-Johnson Syndrome.
Long term use can give rise to a predominantly sensory peripheral neuropathy and cerebellar degeneration.
There may be other reversible changes like gum hypertrophy, acne, hirsutism, and facial coarsening
What do you use for Absent seizures
Ethosuximide
What do you use for focal seizures?
Carbamazapine
What do you use for General seziures?
Valproate
How to test for autonomic neuropathy?
Sweat test and tilt test
Rapidly progressive wide spread weakness and sensory disturbances beginning in the legs …
Gullian Barre Syndrome
In people with Dm, mononeuritis multiplex typically presents as…..
Acute, unilateral and severe thigh pain followed by anterior muscle weakness and loss of knee reflex
neuropathy seen in DM?
- Autonomic neuropathy
- Peripheral neuropathy (Glove and stocking distribution)
- Mononeuropathy - nerve compression or infarct
Infarction of Wernicke’s area leads to…. and which lobe
Receptive aphasia in the temporal lobe
Infarction of broca’s area leads to _____ in which lobe
Expressive aphasia in the frontal lobe
Xanthochromia on LP is indicative of ___
Haemorrhagic stroke - SAH
Causes of SAH?
Rupture berry aneurysm, Aterovenous malformation and trauma
Complications of SAH and what day do they arise (4 of them)?
- Seizures (Day 1)
- Rebleeding (Day 1-2)
- Vasospasm (Day 3)
- Hydrocephalus (Day 1 -7)
Investigations for SAH?
- Non contrast Ct
- LP?
- Angiography?
Intubate when the GCS < ____
8
BP aim in SAH is ______
Systolic: 120-150
Nimodipine is given after SAH because ______
To prevent vasospams
How do you reduce ICP?
Mannitol, put bed at 30 degrees angle and consider a ventricular shunt
headache after blunt trauma, loss of consciousness, ipslateral pupillary dilatation -
Epidural haematoma
CT Brain shows: dense triangle from hyper dense thrombus within the superior sagittal sinus
Venous sinus thrombosis
headache with excessive lacrimation, facial swelling and ptosis
Cluster headache
Paroxysms of severe unilateral pain in the nerve along the face
Trigeminal neuralgia
Acute eye and forehead pain with visual deficits and decreased acuity
Acute angle closure glaucoma
Old female, unilateral blindness, tenderness to temporal area, flu like symtpoms, jaw claudication
Giant cell arteritis (Temporal arteritis) - perform doppler U/S of the temporal artery
Causes of meningitis?
- Strep pneumonia
- Neisseria Meningitides
- H. Influenzae
- Listeria monocytogenes
How does optic neuritis in MS present?
RAPD, Impaired coloured vision, Pain on eye movement, Pale optic disc,
What medications are usedto prevent Migraines?
- BB or TCA
2. Anticonvulsants
A sudural haematoma is between the ____ and _____
Dura and arachnoid mater.
How do you treat trigeminal neuralgia?
carbamazepine
