Neurology Flashcards
Define ISCHEMIC STROKE.
What are the subtypes of ischemic stroke?
Ischemic stroke is defined as reduced perfusion to brain parenchyma as a result of thrombotic or embolic events.
Ischemic stroke can be further divided into:
- thrombotic stroke –> blockage of a vessel due to atheroma
- embolic stroke –> blockage of a vessel due to lodgement of a peripheral emboli (e.g. AF, RHD)
Identify risk factors for ISCHEMIC STROKE.
MODIFIABLE RISK FACTORS ✔️ smoking ✔️ alcohol consumption ✔️ hypertension ✔️ dyslipidemia ✔️ diabetes mellitus ✔️ ischemic heart disease / coronary artery disease ✔️ cardiovascular disease (e.g. AF, RHD, prosthetic valves) ✔️ physical inactivity ✔️ poor diet
NON-MODIFIABLE RISK FACTORS
✔️ increasing age
✔️ male gender
✔️ ethnicity / racial group
✔️ family history of stoke or cardiovascular disease
✔️ personal history of stroke or cardiovascular disease
ANTERIOR CEREBRAL ARTERY (ACA)
✔️ regions supplied
✔️ presenting symptoms
REGIONS SUPPLIED
✔️ medial aspect of the frontal and parietal lobes
✔️ motor homunculus (medially)
✔️ sensory homunculus (medially)
PRESENTING SYMPTOMS
✔️ contralateral lower limb motor deficit
✔️ contralateral lower limb sensory deficit
✔️ urinary incontinence
✔️ confusion, personalty change, poor judgement
✔️ aggression / apathy
MIDDLE CEREBRAL ARTERY (MCA)
✔️ regions supplied
✔️ presenting symptoms
REGIONS SUPPLIED
✔️ lateral aspect of the frontal and temporal lobe
✔️ Broca’s Area (frontal lobe)
✔️ Wernicke’s Area (temporal lobe)
PRESENTING SYMPTOMS ✔️ contralateral upper limb motor deficit ✔️ contralateral upper limb sensory deficit ✔️ unilateral facial paralysis ✔️ dysphasia ✔️ dysphagia ✔️ expressive aphasia (Broca's) ✔️ receptive aphasia (Wernicke's) ✔️ apraxia and sensory neglect
POSTERIOR CEREBRAL ARTERY (PCA)
✔️ regions supplied
✔️ presenting symptoms
REGIONS SUPPLIED
✔️ occipital lobe
✔️ cerebellum
PRESENTING SYMPTOMS ✔️ homonymous hemianopia ✔️ unilateral cortical blindness ✔️ memory loss ✔️ unilateral third nerve palsy ✔️ gait ataxia ✔️ truncal ataxia
Compare UMN versus LMN lesion and relate this to clinical presentation of STROKE.
UPPER MOTOR NEURON LESION ✔️ increased tone ✔️ hyperreflexia ✔️ Babinski's sign +ve ✔️ fasciculations +ve ✔️ muscle wasting absent ✔️ spasticity +ve
LOWER MOTOR NEURON LESION ✔️ reduced tone ✔️ hyporeflexia / absent reflexes ✔️ Babinski's sign -ve ✔️ muscle wasting present ✔️ nil spasticity
Ischemic stroke tends to present as LMN acutely, but progresses to an UMN presentation in its later stages.
TOTAL ANTERIOR CIRCULATION STROKE (TACS)
All THREE of the following are required for diagnosis:
- contralateral upper or lower limb motor or sensory deficit
- homonymous hemianopia
- higher cortical dysfunction (e.g. dysphasia, visuospatial neglect)
PARTIAL ANTERIOR CIRCULATION STROKE (PACS)
TWO of the following are required for diagnosis:
- contralateral upper or lower limb motor or sensory deficit
- homonymous hemianopia
- higher cortical dysfunction (e.g. dysphasia, visuospatial neglect)
LACUNAR STROKE SYNDROME
Any ONE of the following: ✔️ pure sensory stroke ✔️ pure motor stroke ✔️ sensori-motor stroke ✔️ ataxic hemiparesis
POSTERIOR CIRCULATION STROKE (POCS)
Any ONE of the following:
✔️ isolated homonymous hemianopia
✔️ cranial nerve palsy with contralateral motor / sensory deficit
✔️ bilateral motor / sensory deficit
✔️ conjugate eye movement disorder (e.g. nystagmus)
✔️ cerebellar dysfunction (e.g. nystagmus, ataxia)
Identify some clinical signs suggestive of CEREBELLAR STROKE.
✔️ ataxic / broad-based gait ✔️ Romberg's sign POSITIVE ✔️ truncal ataxia ✔️ past-pointing ✔️ DDK ✔️ heel to shin test ✔️ stoccato / slurred speech ✔️ nystagmus (vertical or rotational)
Appropriate investigations for STROKE?
Bedside Ix
✔️ blood glucose levels
✔️ ABG
✔️ ECG
Laboratory Ix ✔️ FBC + WCC differentials ✔️ Inflammatory markers ✔️ UECs ✔️ lipids ✔️ eLFTs ✔️ coags
Imaging Ix
✔️ non-contrast CT brain
✔️ MRI brain (if available –> more sensitive)
✔️ carotid coronary angiogram
Compare treatment of ISCHEMIC versus HAEMORRHAGIC stroke.
ISCHEMIC STROKE
✔️ permissive hypertension (less than 220 / 110mmHg)
✔️ aspirin 300mg PO, stat
✔️ fibrinolytic therapy if < 4.5 hours since symptom onset (once confirmed) –> IV alteplase
✔️ endovascular thrombectomy (if > 4.5 hours since symptom onset)
HAEMORRHAGIC STROKE ✔️ hypotension (<140/90mmHg ideal) ✔️ do NOT give aspirin or anticoagulants ✔️ reverse anticoagulation (if appropriate) ✔️ surgery
Outline clinical presentation for HAEMORRHAGIC STROKE.
✔️ acute onset headache ✔️ loss of consciousness / syncope ✔️ nausea and vomiting ✔️ delirium ✔️ focal or generalised seizures ✔️ neurological deficits
Define TRANSIENT ISCHEMIC ATTACK (TIA).
TIA is defined as transient brain ischemia resulting in neurological deficits that resolve within 24 hours and are NOT accompanied by any permanent brain infarct (as evident on neuroimaging).
It is important to recognise that TIA is a retrospective diagnosis.
Outline the components of the ABCD2 tool and explain its interpretation.
A = age > 60 years (1 point)
B = blood pressure > 140 SBP or > 90 DBP (1 point)
C = clinical features
✔️ unilateral UL or LL weakness (2 points)
✔️ speech impairment without weakness (1 point)
D = duration
✔️ > 60 minutes (2 points)
✔️ 10 to 59 minutes (1 point)
D = diabetes (1 point)
< 4 –> low risk of stroke within next 24 hours
> 4 –> high risk of stroke within next 24 hours (consider hospitalisation + observation)
Describe the management of TIA.
1. Lifestyle modifications ✔️ smoking cessation ✔️ alcohol reduction ✔️ improved physical activity ✔️ hypertension management ✔️ dyslipidemia management
- Antiplatelet therapy
✔️ low-dose aspirin - Anticoagulation
✔️ LMWH (if not contraindications) - Management of co-morbidities
✔️ hypertension –> ACE-I or ARB
✔️ dyslipidemia –> statin
Define INTRACRANIAL PRESSURE (ICP) and identify the three factors that contribute to it.
Intracranial pressure (ICP) is the pressure within the cranium. It is contributed to by:
- brain parenchyma
- CSH
- blood
Normal ICP is between 5 to 10 mmHg.
According to the Munro-Kellie doctorate, an increase in any ONE of the factors that contributes to ICP must be off-set by a decrease in another. This is the principle behind brain herniation.
Define RAISED ICP.
Raised ICP is defined as ICP > 20 mmHg for > 5 minutes.
Identify key clinical features of RAISED ICP.
✔️ headache
✔️ confusion / altered GCS
✔️ nausea and vomiting
✔️ Cushing’s Triad (bradycardia, widened pulse pressure, irregular respiration)
✔️ CNIII compression (unilateral pupillary dilatation, ptosis, “down and out” eye movements)
Outline the principles of NEUROPROTECTIVE RESUSCITATION (management of raised ICP).
CHISSSEL
C = collar off
✔️ remove C-spine collar (if applicable) –> this prevents jugular venous congestion and back-pressure to the brain
H = hypotension, hypothermia, hypoxia AVOID
✔️ aim to maintain a MAP of 80 to 90mmHg
✔️ avoid hypoxia
✔️ keep warm to avoid hypothermia
I = intubate and ventilate
S = sedation
S = seizure prevention
✔️ phenytoin should be given as seizure prophylaxis
S = saline
✔️ 3% hypertonic saline or mannitol should be given
✔️ this increases MAP and draws water out of the brain
E = elevate head to 30°
✔️ assists venous return to the heart from the brain by the effects of gravity
L = last resort is neurosurgery
Identify the three components of the GCS.
GLASGOW COMA SCORE (GCS) is a tool used to assess orientation and consciousness. It is composed of three components:
- eye movements (4 points)
- voice / verbal commands (5 points)
- motor response (6 points)
The highest score is 15. The lowest score is 3 (one point in each of the domains).
A score < 8 is considered a coma.
Describe the scoring system for each of the components of the GCS.
EYE MOVEMENTS 4 points = spontaneous eye opening 3 = opens eyes to voice 2 = opens eyes to pain 1 = does not open eyes
VERBAL RESPONSE 5 = speaking freely, orientated 4 = speaking freely, disorientated 3 = inappropriate words 2 = incomprehensible words 1 = nil words
MOTOR REPONSE 6 = obeys verbal commands 5 = localises to pain 4 = flexion withdrawal 3 = abnormal flexion 2 = extension 1 = no motor response
Define PARKINSON’S DISEASE.
Parkinsons’ Disease is a progressive, degenerative neurological condition characterised by gradual loss of pigmented dopaminergic neurons within the substantia nigra of the basal ganglia.
i.e. reduced dopamine within the substantia nigra.
Identify the hallmark pathological feature of Parkinson’s Disease.
Synuclein-Filled Lewy Bodies within the substantia nigra.
Describe clinical features of PARKINSON’S DISEASE.
Parkinsons’ Disease is characterised by:
- tremour (occurs at rest, alleviated with movement, asymmetric, “pin-rolling…”)
- bradykinesia (slowed movement)
- rigidity (cog-wheel or lead-pipe rigidity)
- mask-like facies
- postural instability
- dementia
- sleep disturbances
- other neurological manifestations (e.g. orthostatic hypotension, oesophageal motility issues, urinary hesitancy / urgency, loss of smell)
Define the diagnostic parameters of PARKINSON’S DISEASE.
Parkinson’s Disease requires BRADYKINESIA plus ONE of the following for a diagnosis:
- rigidity
- resting tremour (between 4 to 6 hZ)
- postural instability NOT contributed to by primary visual, vestibular, cerebellar or proprioceptive dysfunction
LEVODOPA + CARBIDOPA
✔️ mechanism of action
✔️ appropriate dose
✔️ side effects
MECHANISM OF ACTION
Levodopa is a dopamine pre-cursor. It has the ability to cross the blood-brain barrier and be converted into dopamine by the dopamine decarboxylase enzyme. This helps to alleviate the symptoms of Parkinson’s Disease, specially bradykinesia, tremour and rigidity.
Carbidopa is a peripheral dopamine decarboxylase inhibitor. This drug CANNOT cross the blood brain barrier, therefore, remains in peripheral circulation to prevent excessive accumulation of dopamine.
APPROPRIATE DOSE
50mg + 12.5 mg TDS, PO increasing to 100mg + 25mg TDS, PO over 1 to 2 weeks.
SIDE EFFECTS ✔️ psychosis ✔️ poor sleep and vivid dreams ✔️ mood disturbances ✔️ nausea and vomiting ✔️ diarrhoea and constipation ✔️ heart palpitations
Identify three other classes of drugs (besides levodopa + carbidopa) that can be used to treat Parkinsons’ Disease.
- dopamine agonists
- MAO-B inhibitors
- acetylcholine antagonists (e.g. benztropine)
Outline some common complications of Parkinsons’ Disease.
✔️ reduced independence with activity of daily living
✔️ increased reliance on others (family members, carers etc).
✔️ dementia (particularly Lewy Body)
✔️ depression
✔️ aspiration pneumonia
✔️ increased cardiovascular risk
✔️ death
Define DEMENTIA. Identify some common sub-types of dementia.
Dementia is a progressive and non-reversible reduction in cognition, executive functioning, speech and language, memory and visuospatial awareness.
It is an umbrella term that encompasses multiple conditions characterised by a similar cognitive decline.
Subtypes of dementia include: ✔️ Alzheimer's Disease ✔️ vascular dementia ✔️ Pick's Disease / frontotemporal dementia ✔️ Lewy Body dementia ✔️ Parkinson's Disease ✔️ Motor Neuron Disease
DEFINE the FOUR A’s of DEMENTIA.
- amnesia: difficulty with memory (long or short term)
- agnosia: difficulty recognising familiar faces / objects
- apraxia: difficulty with coordinated movements
- aphasia: difficulty with communication and speech
Identify Ddx for CONFUSION in an older person.
✔️ dementia ✔️ delirium ✔️ depression ✔️ drugs ✔️ subdural hematoma (acute, subacute or chronic)
Outline appropriante investigations for CONFUSION.
Bedside Ix
✔️ urine dipstick + urine MCS
✔️ blood glucose levels
Laboratory Ix ✔️ FBC + WCC ✔️ Inflammatory markers ✔️ UECs ✔️ eLFTs ✔️ coags ✔️ TFTs ✔️ Iron studies + B12 + folate ✔️ syphilis serology ✔️ blood glucose level ✔️ blood culture (if sepsis suspected) ✔️ toxicology (?)
Imaging Ix
✔️ non-contrast CT head
✔️ CXR / chest CT
Outline some NON-PHARMACOLOGICAL management options for DEMENTIA.
EDUCATION
✔️ provide adequate education to the patient and their family
✔️ refer to a support group
✔️ refer to a dementia specialist (e.g. psychology services)
ENVIONRMENT
✔️ encourage patient to stay in a familiar environment for as long as possible (e.g. their home)
✔️ time-orientating cues
✔️ familiar faces (e.g. family members, carers)
✔️ establish a routine
DRUGS AND MEDICATIONS
✔️ cease any non-essential medications
✔️ cease or change any medications that may contribute to BPSD or delirium
GENERAL HEALTH ✔️ optimise general health and wellbeing ✔️ manage other medical conditions appropriately ✔️ encourage physical activity ✔️ smoking cessation ✔️ reduce alcohol consumption
Identify pharmacological options appropriate for the management of dementia.
- acetylcholinesterase inhibitors –> help improve symptoms in the short term; do not address the underlying degenerative nature of the disease
- antidepressants –> improve / alleviate mood symptoms
- atypical antipsychotics –> behavioural and psychotic symptoms of dementia
- benzodiazepines –> can assist with acute aggression / agitation
Define BEHAVIOURAL AND PSYCHOTIC SYMPTOMS OF DEMENTIA (BPSD) and identify some of the most common.
BPSD are common complaints in the end stages of dementia. The most common presentations include:
✔️ hallucinations (e.g. visual, auditory)
✔️ delusions
✔️ aggression and agitation
✔️ depression and anxiety
✔️ apathy and disinhibition
✔️ irritability or indifference
✔️ “twightlighting”
✔️ night time behaviours (e.g. wandering)
BPSD require both pharmacological and non-pharmacological interventions.
Define DELIRIUM.
Delirium is a transient and reversible reduction in consciousness / orientation and awareness / cognition. It is usually of an acute onset and can be treated.
Outline the most common causes of DELIRIUM.
D = drugs (e.g. medications, drug intoxication, drug withdrawals)
E = electrolyte imbalances (e.g. hyponatremia, hypokalaemia, magnesium, calcium and phosphate)
L = low oxygen (e.g. anaemia, hypoxia, congestive cardiac failure)
I = infection (e.g. UTI, pneumonia)
R = retention (e.g. urinary, fecal)
I = increased ICP (e.g. malignancy, tumour, bleed)
U = uremia
M = metabolic (e.g. low blood glucose, thyroid dysfunction)
Identify some appropriate investigations for DELIRIUM.
Bedside Ix
✔️ blood glucose level
✔️ urine dipstick + MCS
✔️ ECG
Laboratory Ix ✔️ FBC + WCC ✔️ ESR + CRP ✔️ UECs ✔️ blood culture ✔️ iron studies + B12 + folate ✔️ CMP
Imaging Ix
✔️ CXR
✔️ abdo XR
✔️ non-contrast CTB or MRI
Describe appropriate management options for DELIRIUM.
- Identify and treat / reverse the underlying cause (if possible).
- Keep the patient in a quiet and well-lit room.
- Space and time orientating features should be present.
- Optimise hearing and vision.
- Have a family member / support person close by for familiarity.
- Continually re-assess the patient to ensure no important diagnoses have been missed.
- Avoid using benzodiazepines.
- Consider atypical antipsychotics, including:
✔️ olanzapine
✔️ risperidone
✔️ haloperidol
Define GULLIAN BARRE SYNDROME (GBS).
GBS is a believed to be an auto-immune mediated polyneuropathy that occurs following viral infection. It is acute, rapidly progressive but usually self-limiting.
GBS is an example of a LOWER MOTOR NEURON disease.
Describe key clinical features of GBS.
✔️ symmetrical flaccid paralysis ✔️ loss of sensation distally ✔️ loss of deep tendon reflexes ✔️ facial and oropharyngeal involvement in 50% of cases ✔️ respiratory paralysis in 10% of cases
Differential diagnoses for GBS?
✔️ myasthenia gravis
✔️ botulism toxin
✔️ poliomyelitis
✔️ tick paralysis
Management of GBS?
IV immunoglobulin is the first-line treatment for GBS. Do NOT give corticosteroids, as these usually worsen the disease progression.
Define MYASTHENIA GRAVIS.
Myasthenia gravis is an autoimmune condition in which autoantibodies are produced against the acetyl choline receptor at the neuromuscular junction. This leads to early activation at the NMJ and inadequate muscle contraction with nerve stimulation.
Describe key clinical features of MYASTHENIA GRAVIS.
✔️ symmetrical fatiguable muscle contraction –> NOT associated with sensory changes, changes to reflexes or abnormalities with coordination
✔️ ptosis
✔️ dysarthria or dysphagia
✔️ respiratory muscle weakness –> may lead to respiratory failure
Outline key tests for MYASTHENIA GRAVIS.
- Endophonium test –> endophonium is an acetyl cholinesterase inhibitor; prolongs the presence of acetyl choline within the synaptic cleft of the NMJ and temporarily alleviates symptoms
- anti-ACh-R autoantibodies
- anti-musK autoantibodies
- chest CT / MRI (85% of patients with MG have thymic hyperplasia)
- spirometry –> used to assess forced vital capacity over time
Outline appropriate management of MYASTHENIA GRAVIS.
✔️ thymectomy --> around 85% of patients achieve remission afterwards ✔️ corticosteroids ✔️ IV immunoglobulin ✔️ anti-cholinesterase inhibitors ✔️ symptomatic relief
Define BELL’S PALSY.
Bell’s Palsy is a neurological condition characterised by acute onset, unilateral lower motor neuron weakness of the facial nerve in the absence of an identifiable cause.
The exact pathophysiology is unknown; believed to be related to auto-immune inflammation post-viral infection.
Outline key features of BELL’S PALSY.
✔️ unilateral facial drooping and muscle weakness (no sparing of the forehead)
✔️ dryness of the eye and mouth
✔️ taste disturbances
✔️ hyperacusis
What is the appropriate management of BELL’S PALSY?
Corticosteroids.
What is the clinical triad characterised of MULTIPLE SCLEROSIS?
- Nystagmus
- Intention tremor
- Scanning speech
Outline / describe key features of MULTIPLE SCLEROSIS.
✔️ blurred vision (optic neuritis)
✔️ limb weakness / paraesthesia without autonomic dysfunction
✔️ ataxia, facial numbness, diplopia
✔️ first episode of trigeminal neuralgia
✔️hemiplegia
✔️ tingling in spine of limb / neck flexion (Lhermitte’s Phenomenon)
✔️tonic spasms
Define MULIPLE SCLEROSIS.
Multiple sclerosis (MS) is a chronic, degenerative disorder of the CNS, characterised by immune-mediated inflammatory process. This process results in demyelination of the white matter within the spinal cord and brain.
