Neurology Flashcards

1
Q

A-What is Syringomyelia?

B-Where is it most common?

C-What is the most common cause of Syringomyelia?

A

A-Syrinx= tube. So its the formation of a tube at the centre of the spinal cord that’s expansile & contains fluid.

B-Cervical area or C8-T1.

C-Anything that obstructs the flow of CSF. Most common is= chiari malformation (the herniation of the cerebellum (cerebellum tonsilar herniation) through foramen magnum because of abnormal skull shape that doesnt accommodate for space which can be acquired through trauma OR congenital).

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2
Q

A-How does Syringomyelia presents?

B-What if the syrinx expands to the brainstem?

C-What if it expands to the dorsal column?

A

A-Expansile character= destroys the spinothalamic tract (pain & temp + crude touch) + incidious onset then rapid progression of symptoms.

Presentation: Cape-like bilateral pain & temp. If it expands further to the anterior horn cells= weakness & atrophy of the hands.

B-Horner’s syndrome & CN palsies. will be called Syringobulbia.

C-Proprioception/vibration/light touch will start to get affected.

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3
Q

Lumbar Spine stenosis:

What is it & what are the causes?

A

Narrowing of the spinal canal (space that cord runs through).

Most common cause: degenerative changes (e.g. facet joint oesteoarthritis forms osteophytes and articular cartilage erosion which mechanically compress & narrows the canal). Other causes: Tumors, disc prolapse.

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4
Q

A-Symptoms & signs of Lumbar spine stenosis?

B-Diagnosis?

C-Mx?

A

A-POSITIONAL element of lowerback/buttock/lower limb pain (better when sitting, walking uphill, leaning forward as the canal enlarges & relieves the stenosis. Worst when walking). Numbness & paresthesia.

B-MRI spine

C-Weight loss, NSAIDs, PT, Decompressive laminectomy.

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5
Q

Prolapsed Intervertebral Disc (slipped disc):
A- What happens in pathophysiology?

B-Which position does herniation occur?

C-Risk factors?

D-Common sites?

A

A-Tear in annulus fibrosus= nucleus pulposes bulges out= impinges on a spinal nerve.

B-Postero-lateral (posterior long. ligament prevent direct posterior herniation which will impact the spinal cord rather than nerve).

C-Heavy lifting, sport trauma, disc degeneration, idiopathic.

D-L4/L5 or L5/S1

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6
Q

A-What’s Beck’s Syndrome (Anterior spinal artery occlusion/syndrome)?

B-Signs & Symptoms?

A

A-Infarct of anterior 2/3 of the spinal cord. Causes= Aortic pathology e.g. Aneurysm or dissection

B-1) Loss of pain & temp (spinothalamic=anterior cord) below the lesion
2) loss of bilateral motor command: UMN below the lesion, LMN at the level of the lesion

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7
Q

Brown-Sequard Syndrome:

A-How does this condition develop?

B-Signs & Symptoms?

A

A-Insult to one lateral half of the spinal cord (Hemisection)

B-1) Ipsilateral loss of all sensation at the level of lesion

2) Ipsilateral loss of proprioception & vibration below the lesion.
3) Contralateral loss of pain & temp below the lesion.
4) Ipsilateral loss of LMN at the level of lesion (flacid paralysis)
5) Ipsilateral UMN signs below the lesion
6) if lesion above T1= horner’s syndrome (Oculosympathetic pathway)

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8
Q

When you are presented with signs of LMN, what would you want to exclude for differentials?

A

That its a neuropathy rather than myopathy (primary muscle disease)

Primary Muscle Disease:
1-Symmetrical weakness usually proximal (e.g. getting dressed, brushing teeth)
2-Late loss of reflexes compared to neuropathy
3-No sensory loss

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9
Q

What disorders might cause a mixture of UMN and LMN signs?

A

Motor Neuron Disease: its a neurological condition of unknown cause which can present with both UMN and LMN signs.

e.g. Amytrophic lateral sclerosis (50% of patients), primary lateral sclerosis, progressive muscular atrophy, progressive bulbar palsy.

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10
Q
What are the specific patterns of motor loss in the following:
1-Cortical lesions
2-Internal capsule
3-Corticospinal tract
4-Cord lesions
5-Peripheral neuropathies
A

1-Cortical lesions: unexpected pattern of weakness of all movemments of hands or foot, normal or reduced tone, high reflexes proximally (suggest UML not LMN)
2-Internal capsule and 3-Corticospinal tract: contralateral hemiparesis (if occurs with epilepsy, reduced cognition or homonymous hemianopia= lesion is in cerebral hemisphere)
3-Cord Lesion: Paraparesis, Quadriparesis, tetraplegia. If it’s UMN then signs below lesion. If LMN the sign at the level of the lesion.
4-Peripheral Neuropathies (include polyneuropathies & mononeuropathies): Polyneuropathies have distal weakness e.g. Foot Drop, Wrist Drop (e.g. GBS).
B-Mononeuropathy: Trauma or entrapment e.g. Carpel Tunnel.

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11
Q

What patterns can weakness present as?

A

UMN Lesions:
Damage to the motor pathways (corticospinal tracts also sometimes called pyramidal tract) anywhere from motor nerve cells in the precentral gyrus of the frontal cortex> internal capsule> brainstem>cord>synapse with anterior horn cells in cord.

LMN Lesions:

Damage of the motor pathways anywhere from anterior horn cells in the cord>nerve roots> plexi>peripheral nerves.

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12
Q

What are the signs of UMN Lesions?

A

1-UMN lesions affect MUSCLE GROUPS (not individual muscles)
2-Pyramidal pattern weakness:

Upper limb flexed with weakness of: shoulder abduction>adduction, Elbow extension>flexion, wrist dorsiflexion>volar flexion, finger abduction>adduction.
Lower limb extended with weakness of: Knee flexion>extension, Ankle dorsiflexion>plantar flexion, foot eversion>inversion.
Foot plantar is flexed and supinated (inverted)
Circumductive gait

3-No muscle wasting
4-loss of skilled fine finger movements
5-Spasticity in stronger muscles (arm flexors and leg extensors)- High tone thats velocity dependent and non-uniform)= CLASP KNIFE
6-Hyperreflexia
7-+Ve Babinski sign
8-Clonus (>3 rhythmic downwards beats)
9-+Hoffman’s reflex- brief flexion of thumb and index finger in a pincer movement following a flick to the middle finger.

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13
Q

What are the signs of LMN Lesions?

A

1-Distribution of weakness corresponds to those muscles supplied by cord segment, nerve root, plexus, or peripheral nerve.
2-wasting and fasciculations (spontaneous involuntary twitching) of affected muscles.
3-Hypoflaccidity/hypotonia
4-Reduced/absent reflexes
5-Plantars remain flexor

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14
Q

What are some pathological Gait abnormalities?

A

1-Antalgic Gait: Due to pain in 1 area, tends to put one leg down for a shorter time than the other creating an assymmetrical gait.

2-Ataxic (broad-based gait): Due to Cerebellar Lesion or Alcohol. Unable to walk Heel-To-Toe.

3-Shuffling (Festinating Gait/Gait Apraxia): extra-pyramidal disease.

4-Tilted Gait: Inner Ear disorder

5-High-Stepping Gait: Foot-Drop— a person will lift their foot far above the ground in order to avoid catching their toes on the ground while walking. They will also have difficulty walking on their heels.

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15
Q

What’s Parkinson’s Disease definition?

A

Neurodegenerative disease. Degeneration of dopaminergic neurons in the substantia Nigra. More common in men age 65. - Able to see lewy bodies as hallmark of parkinson’s in Substantia Nigra.

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16
Q

What are the cardinal TRIAD symptoms of PD?

A

1-Tremor: Resting tremor which is worst on one side, can be bilateral or even involve the legs. Pin-rolling. Its worst when arm isnt being used or patient is anxious.
2-Bradykinesia: short, shuffling steps with reduced arm swinging. Difficulty initiating movement, hypokinesia.
3- Rigidity: lead pipe & cogwheeling (due to superimposed tremor).

  • Asymmetry as characteristic of PD symptoms.
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17
Q

Other motor symptoms of PD?

A

Mask-like facies
Flexed posture
Micrographia

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18
Q

Causes of PD?

A

1-Idiopathic PD- 70%
2- Parkinsonian plus: MSA (Multiple System Atrophy), PSP (Progressive Supranuclear Palsy), CBS (CorticoBasal Syndrome)
3-Dementia with lewy bodies
4-Drug-Induced Parkinsonism (rapid-onset): Neuroleptics: Haloperidol, Risperidone, Anti-Emetics: Metoclopramide, Prochlorerazine (NOT domperidone)
5-Toxication: Manganese or copper (wilson’s), carbon monoxide
6-Post-Infectious: flu, HIV, encephalitis
7-Trauma: boxing (dementia -pugilistica)
8-Vascular: DM or HTN
9-Genetics

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19
Q

When Investigating PD via Hx, you want to ask the triad + other motor symptoms + non-motor symptoms:

What are the non-motor symptoms?

A

Non-Motor symptoms:

1-Visual Hallucinations
2-Mood: depression & dementia & psychosis
3-Postural hypotension (autonomic dysfunction)
4- REM sleep disturbances
5-Restless leg syndrome
6-Constipation (autonomic dysfunction)
7-Urinary: frequency & urgency 
8-Fatigue
9- Back & Neck pain 
10- Loss of sense of smell 
11- Dribbling of saliva

*If cognitive dysfunction (dementia) starts early (usually late) then it might be lewy body dementia than PD.

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20
Q

Is it parkinson’s Plus syndrome? 5 VIVID red flags:

A

1-Early postural instability & Vertical gaze palsy down (gaze worse than up gaze so they might complain of difficulty reading or descending stairs)+/- falls, rigidity of trunk > limbs, Symmetrical onset, speech & swallowing problems, little tremor = PSP (poor response to L-Dopa)
2-Early autonomic features e.g. Impotence/incontinence, postural hypotension, cerebrall + pyramidal signs (DANISH), rigidity > tremor = MSA
3- Fluctuating cognition with Visual hallucinations & early dementia = Lewy Body Dementia
4-Akinetic rigidity involving 1 limb, cortical sensory loss (e.g. astereognosis), apraxia (even autonomous Interfering activity by affected limb-the alien limb phenomenon) = CBS
5-Pyramidal signs (legs) e.g. Diabetic/hypertensive patient who falls or has gait problems e.g. ataxia (no festination) = vascular parkinsonism

21
Q

Can depression cause parkinsonism?

A

Severe psychomotor retardation associated with depression can give a parkinsonian appearance, with slow movements and loss of facial expression.

22
Q

PD Treatment options available?

A

Aim: to increase dopamine level in CNS. Dopamine itself cant cross the BBB!

1-Levodopa: Is a dopamine precurser able to cross the BBB to the brain. Once in, its converted to Dopamine by Dopa Decarboxylase found within the remaining niagra stria. neurons. On its own there’s Intestinal (jejunal) gel infusion.

2-Dopa Decarboxylase inhibitor (Carbidopa): There is peripheral dopa decarboxylase which is able to convert Levodopa > Dopamine > Epinephrine (arrhythmias) before crossing BBB. SO Carbidopa is given with Levodopa in the following mixtures: 1-Co-Beneldopa (Madopar) 2-Co-Careldopa (Sinemet)

3-Dopamine agonist: Stimulates the dopamine receptors ti think there’s more dopamine. Ergots: Bromocriptine, Carbergoline, Pergolide. Not Ergot: Pramipexole, Ropinirole

4-Apomorphine: none-selective dopamine agonist (DA infusion)

5-Anti-cholinergics: In CNS, When dopamine levels is reduced, ACh levels increase in proportion. SO Anti-cholingerics restore the balance b/w dopamine & ACh signaling in the brain.
procyclidine, benzotropine, trihexyphenidyl (benzhexol)

6-MAO-B Inhibitors: MAO degrades Dopamine. Selegiline, Rasagiline.

7-COMT Inhibitors: COMT is an enzyme that degrades Dopamine. Entacapone, Tolcapone

8-Deep brain stimulation (DBS): Implanted device that directly sends signals to basal ganglia = counteracts aberrant signaling.

23
Q

PD Principles of management?

A
  • In practice, clinicians often start patients on DA (non-ergot derived) first or MAO-B inhibitors to reserve Levodopa because once started its effect gradually decline in 15 years.

1st ) Initially: Motor symptoms: Levodopa
Non-Motor symptoms: Levodopa, DA, MAO-B inhibitors

2nd) Symptoms cont. despite Levodopa or they develop dyskinesia: Add adjunct: DA, MAO-B Inhibitors, COMT inhibitor
3rd) Consider others: Apomorphine infusion, DBS, Intestinal gel levodopa infusion

24
Q

Side Effects of: A)Levodopa B) DA

A

A) Levodopa: drug-induced Dyskinesia (at end of dose) - Arrhythmias - Postural hypotension - Nausea & Vomiting- Dry mouth - Psychosis- Drowsiness

B) DA: excessive day time Sleepiness, hallucinations (more than Levodopa in older people), impulse-control problems, postural hypotension, nasal congestion

25
Q

How to manage PD postural hypotension?

A

Look at medications that might be worstening it.

Treat with Midodrine (inc. arterial resistence by acting on peripheral alpha-adrenergic receptors)

26
Q

How to manage PD excessive day-time sleepiness?

A

Dont drive. Give: Modafinil

27
Q

How to manage PD saliva drooling?

A

Glycopyrronium bromide

28
Q

What happen if a PD patient is non-compliant or the medication isnt absorbed?

A

1- Acute Akinesia
2-Neuroleptic Malignant Syndrome: pyrexia, rigidity, tachycardia = Inc. Creatine Kinase. Usually happens >10 days of initiating or stopping drug. Treat with: IV Benzodiazepine or Dantrolene

29
Q

Ix of PD?

A

DAT scan: dopamine associated transporter
MRI:
MIBG:

30
Q

MS definition:

A

Chronic Central Demyelination (autoimmune process- T-cell mediated antibodies cross the BBB from peripheries to attack the brain, optic & spinal cord in a plaque pattern).
Myelin & sometimes axons are attacked but the cells that make myelin (glial cells) are not attacked so gives it the relapsing/remitting nature). Unfortunetly progressive axonal loss = progressive clinical symptoms.

31
Q

Epidemiology or risk factors of MS:

A

F>M x3, 20-40yrs (mean 30yrs), higher prevalance further from the equator so more common in whites.
Risk Factors: genetic susptibility (Fhx of autoimmune diseases) , Vit. D early life exposure including maternal, Distance from equator. including migration, Viral: EPV,HHV6, Chlamydia, Pneumonia.

32
Q

Types of MS:

A

1-Relapsing Remitting- seen in younger patients first Dx- Treatment tries to redce frequency & duration of relapses.
2-Primary Progressive- seen in older patients first Dx.
3-Secondary progressive- usually after long period of relapsing & remitting. This is what Mx tries to prevent!

33
Q

Clinical Features of MS (wide variety due to locations of demyelination):

A

Visual:
1- Optic Neuritis (inflammatory demyelination of optic nerve): Monosymptomatic/unilateral -Retro bulbar Pain (discomfort behind the affected eye esp. In eye movement) -Blurred vision - Loss of colored vision & reduced light perception. O/E: reduced Acuity & color vision - Pink swollen optic disc acutely - Visual field defect (central scotoma) - RAPD/ Marcus gunn pupils - INO

2-Optic Atrophy: Pale optic disc (chronically)
3-Uhthoff’s phenomenon: worsened vision after inc. body temp. (fever, hot baths, hot climate, vigerious exercise)
4-Hemianopia

Sensory: 
1- reduced vibration & proprioception: 
2-Pins & Needles 
3-Lhermilte's sign: When neck flexes, theres shooting pain down the spine & peripherally towards lower limbs (cervical vertebrae demyelination).  
4-Chronic neuropathic pain
5-Trigeminal neuralgia
6-Swallowing difficulty & Constipation

Motor:

  • Spastic weakness: UMN spastic weakness of feet causes FOOT DROP so patients circumflex their gait which affects hips. Solution= LMN electric stimulation of common perinoeal nerve to dorsiflex as they step. Also on examination= BRISK reflexes because its UMN
  • Chronic fatigue
  • Myelitis (transverse)

Cerebellar:

  • Ataxia (incoordination)
  • Nystagmus (oscillopsia): visual fields oscillate-disabling in terms of reading & when trying to focus on things like dressing & mechanic work.
  • Dysarthria (slurred-speech)
  • Intentional tremor
  • Diplopia

Other:

  • Urinary symptoms: urinary retetion or increased frequency & urgency, overflow or incontinence
  • Sexual dysfunction: Erectile dysfunction, anorgasmia
  • Intellectual deterioration/Cognitive dysfunction: Frontal lobe Executive dysfunction (attention, decision making, working memory), Dementia, Depression, Mental fatigue
34
Q

How to diagnose & Ix MS?

A

Its important to remember that MS diagnosis is CLINICAL as there isnt a pathognomonic test specific to MS. Diagnosis is made: lesions disseminated in time & space (2 or > attacks of 2 different parts of the CNS) that are unattributable to other causes e.g. cord compression (SO after first episode further evidence is needed however a careful history might suggest previous episodes e.g. unexplained brief vision loss). Also if someone presents with 1st episode 7 you go ahead to do MRI in which lesions/plaques are found then 90% of patients do go on to develop MS).

MRI Flair sequence: multifocal hyperintense cortical lesions & periventrically (within ventricles). *Note: These lesions can be viewed despite remission which contributes to cortical cognition dysfunction (executive processing & working memory). This indicates that theres an invisible chronic process going on so itsa cue to titrate the medication up for patients.
Other MRI: T2 MRI (less lesions detected). MR is sensitive for plaque detection, but the appearances are non-specific (e.g. ischaemia, vasculitis) and MR severity of disease does not correlate well with clinical findings.

LP CSF Sample: detects oligoclonal bands/microfilaments of IgG on electophoresis that are no detected in serum (CNS inflammation).

Evoked Potentials: delayed/ slow conduction speed but well preserved waveform (visual, auditory & somatosensory).

35
Q

General MS workout bloods?

A
  • FBC, WCC, Vitamine B12
  • Lupus antibodies:
  • ESR & CRP: to see if systemic inflammatory condition
  • HIV & Syhphilis: mimic MS
  • CXR: Sarcoidosis
36
Q

Management of MS Acute Flair + Chronic ongoing management?

A

Acute Relapse: High doze steroids- Oral or IV methylprednisolone for 5days (it only shortens the duration of relapse)

Disease Modifying drugs:
Beta-Interferone: reduces relapse by 30%
Criteria met before use: 1) R-R disease + 2 relapses in past 2yrs + can walk 100m unaided
2) secondary progressive disease + 2 relapses in past 2yrs + can walk 10m unaided or aided.

Glatiramer acetate: immunomodulating drug acts as immune decoy
Natalizumab: monoclonal antibody- antagonises migration of leukocytes across epithelium across BBB.
Fingolimod: Spihnosine 1-phosphate receptor modulator: prevents lymphocytes from leaving lymph nodes.

37
Q

Management of these specific MS symptoms: Fatigue, Spasticity, Bladder Dysfunction, Oscillopsia?

A

Fatigue: Trial of amantadine, Mindfulness & CBT
Spasticity: Baclofen & Gabapentin (doesnt work well) first-line. Other: Diazepam. Dantrolene, Tizanidine. Botulen injection (targets localised spasticity e.g feet inversed), Interthecal baclofen pump (goes into CSF needle & release baclofen periodically- Last resort).
Bladder dysfunction: Get USS to assess bladder emptying. Avoid anti-cholinergics as worsens symptoms in some patients.
-If significant residual volume = Intermittent self-catheterisation. If no significant residual volume = Anti-cholinergics (oxybutinine/tolterodine) to inc. urinary frequency.
-Oscillopsia: Gabapentin

38
Q

Q: Someone admitted with seizures, is convulsing. What’s the immediate management?

A

The most pressing consideration here is to stop the seizure and prevent hypoxic brain injury. Once fitting is controlled then exploration of the underlying cause can be explored.

Airway, breathing and circulation is essential and, once IV access established, a bolus dose of benzodiazepine (e.g. Lorazepam 4mg) can be given over 2 minutes.

Hypoglycaemia is an important treatable cause of seizures and if convulsion continues infusion of glucose solution should be considered while awaiting blood glucose result.

Other things: Time the seizure, Padded bed rails (dont restrain), administer O2, place them semi-prone to prevent aspiration. Check if alcoholic or nutritional status to adminster Pabrinex before glucose.

Also: If no IV access: Buccal Midazolam.

(can repeat a 2nd dose within 10-20mins)

-If no previous epilepsy→ Urgent CT, Alert Anesthetist and ICU.

39
Q

The patient has stopped convulsing after Lorazepam 4mg IV, and is post-ictal. What will you do?

A

Blood screen is now needed (including calcium) once patient stabilised. ECG is required to exclude arrhythmia. Collateral history and further examination are essential.

Bloods: FBC, U&E, LFT’s, Glucose, Calcium, Magnesium
ABG
ECG
Urine dip: toxicology
Physical examination & Obs + set up cardiac monitor & pulse oximetry
Take collateral Hx

40
Q

If the patient is at high risk of recurrent seizure (e.g brain mets) or has entered status epilepticus, what would you do?

A

Alert Anesthetist

-IV infusion of 2nd line Anti-Epileptic Agent (1 of the following):

1-Phenytoin
2-Valproate
3-Levetiracetam

Anaesthetist then can manage:-General Anesthesia for 12-24hrs:

1-Propofol
2-Midazolam
3-Thiopental Sodium

  • Anaesthetics can help in obtaining CT Brain, using a portable CXR as well
41
Q

Someone has brain mets & had seizure, what would you do?

A

Contraindicated LP in space-occupying lesions, steroids help reduce cerebral oedema around the lesions. You will liase with oncologist/radiotherapist, consider staging CT or FDG PET. Analgesia as needed.

42
Q

Stroke: Definition, 2 types, risk factors?

A

Interruption to blood supply causing sudden onset of neuro deficits for >24hr or causing death

•	Two types
o	Ischaemic (70%)
	Atheroembolism
	Cardioembolism
	Intracranial small vessel disease
-Can also be from hypo perfusion & stenosis of vessels. 
o	Haemorrhagic (15%) (intracranial H. or Subarachnoid H.) caused by: 
	Hypertension (pops the blood vessel)
	Anticoagulation
	Head injury
	Berry aneurysm (associated with PCKD)
•	Risk factors: Same as IHD
o	Diabetes
o	HTN (the most associated factor with stroke – most important to reduce BP!)
o	Hypercholesterolaemia
o	Smoking
43
Q

We usually divide the intracranial arteries into 2 general vascular territories: anterior & posterior. List what constitutes in each territory:

A

Anterior part of the brain (carotid):

1-Opthalmic (amaurosis fugax, branch or central retinal artery occlusion) Note: the eye is part of the brain
2-Anterior Cerebral (ACA)
3-Middle cerebral (MCA)

Posterior (vertebrobasilar):

1-Basilar (brainstem)
2-Cerebellar arteries (SCA, AICA,PICA)
3-Posterior cerebral (PCA)

44
Q

There are 2 known classifications of stroke symptoms, Outline the oxford Classification of Ischemic Stroke (according to the vascular terriroty affected):

A

• Total anterior circulation infarct (TACI) (carotid): ALL 3 (only one of higher dysfunc needed)
o Higher dysfunction (speech, vision, consciousness deficits)
 Dysphasia (NB: 95% of people, irrespective of hand, have broca/wernicke on LEFT)
 Visuospatial defects (e.g. neglect)
 Decreased LoC
o Homonymous hemianopia
o Motor and sensory defects (face, arm, leg)

• Partial anterior circulation infarct (PACI (carotid): 2/3 of TACS, or higher dysfunction alone
o Higher dysfunction alone
o High dysfunction + hom hemi
o High dysfunction + Partial mot/sens
o Homonymous hemianopia + Partial motor or sensory defect (with NO higher dysfunction)

• LACS/Lacunar (intrinsic small vessels [perforating arterioles] – NO higher dysfunction whatsoever)
o Pure motor  Face AND arms AND legs
o Pure sensory
o Sensorimotor
o Ataxic hemiplegic  Weakness + ataxia affecting IPSILAT side
 AKA “Dysarthria-clumsy hand” Syndrome

• Posterior circulation infarct ( POCS (vertebrobasilar):
o Cerebellar dysfunction (DANISH)
o Cranial nerve palsy (CN3,5,7,8) + contralateral motor/sensory deficit
o Unilateral/bilateral motor and sensory deficit
o Isolated homonymous hemianopia (occipital lobe)
o Cortical blindness (basilar artery occlusion)

45
Q

Initial Mx of suspected stroke?

A

o Initial test: non-contrast CT head

o	After CT head: 
	Haemorrhagic
•	STOP ANTICOAGULANTS. Reverse as necessary
•	Lower BP
•	NEUROSURGERY REFERRAL (poor prognosis)

 Ischaemic (may not see any CT signs, must use clinical judgement)
• LESS THAN 4.5hrs
o Consider thrombolysis

• If MORE THAN 4.5hrs from onset
o Aspirin 300mg

46
Q

For patient with infarct stroke <4.5hrs, they often get thrombolysis (e.g. alteplase), but what are the CI for it?

A

Absolute CI:

  • Previous Intracranial Haemorrhage
  • Seizure at onset of stroke
  • Intracranial neoplasm
  • Stroke or trauma to the head/brain in last 3m
  • LP in past 7 days
  • Suspected SAH
  • Active bleeding
  • Pregnancy
  • GI bleeding in past 3w
  • Oesophageal varices
  • Uncontrolled HTN >200/120mmHg

Relative CI:

  • Concurrent Anticoagulation (INR>1.7)
  • Bleeding disorders
  • Active diabetic haemorrhagic retinopathy
  • Suspected IntraCardiac thrombus
  • Major surgery or trauma in past 2w
47
Q

What is the secondary Mx of stroke?

A

o First: Investigate
o ECG  AFib?

o Echocardiogram

o Carotid Doppler USS  Carotid endarterectomy in <1wk
 Indications for Carotid endarterectomy:
• >70% stenosis

o Second:
 Everyone: Modify cardiac risk

 Anticoagulation:
• No A-Fib: Aspirin 300mg x2wk, then Clopidogrel 75mg long-term + MR (modified-release) Dipyridamole

• A-Fib: Aspirin 300mg x2wk, then Warfarin

48
Q

DDx for stroke mimics, and fastest way to differentiate from stroke?

A
1-Hypoglycaemia 
2-Migraine
3-Epilepsy
4-MS
5-Brain tumours
6-Syncope
7-CNS infections: encephalitis, meningitis
8-Head Injury

Stroke: negative symptoms e.g. losing speech, power
Stroke mimics: Positive symptoms e.g. tingling, visual aura

Onset timing is also important. Stroke= abrupt onset.

49
Q

When is thrombectomy recommended for acute ischemic stroke?

A

If the CT perfusion scan or diffusion-weighted MRI sequence shows a limited infarct core (with the potential to salvage affected brain tissue), they should be offered thrombectomy between 6-24 hours after the event