Neuro SAQ Flashcards
Young man with acute GE, afterwards present with LL weakness + arreflexia, ascending to affect upper limbs.
- What is your diagnosis (1)
2.What tests to support your diagnosis (3) - After admission, the patient then developed ataxia + bilateral partial ptosis. Name the condition (1)
- What antibody is associated with this condition? (1)
- 2 Complications potentially associated with “this condition that the patient has developed” (2)
- GBS
- LP for CSF cytoalbuminologic dissociation, NCS, anti ganglioside ab, EMG
- Miller fisher syndrome
- Anti- ganglioside antibodies (GQ1b)
- Autonomic dysfunction, paralytic ileus, urinary retention, respiratory failure, dysphagia (bulbar dysfunction)
- IVIG, plasma exchange
A middle-aged woman went to Japan, and she had mild flu-like symptoms during the trip. 2 weeks later she developed fever, confusion and speech problems. Physical examination revealed four limbs with normal power, no focal neurological deficits. History of depression, asthma, severe eczema, iatrogenic adrenal insufficiency.
1. Most likely dx and possible ddx
Plain CT show hypodensity over left side, sulcal effacement, obliteration temporal horn of lateral ventricle. Contrast MRI confirm same finding, and an additional area over right side, contrast enhancing over temporal area.
2. What specific investigation and treatment do you want to do. Briefly describe rationale
Suddenly deteriorate, left eye ptosis and abducted, right hemiparesis, CT showed same picture but with more extensive involvement.
3. what happened and what is your management
- Viral encephalitis, metabolic encephalopathy, autoimmune/post infective encephalitis, addisonian crisis, other infectious causes (bacterial, TB, fungal)
- Blood for viral PCR
CSF for differential cell count, protein, glucose
CSF for PCR HSV1/2, VZV, enterovirus, IgM JE
NPA x respiratory panel
EEG
IV acyclovir - Cerebral edema causing raised ICP and uncal herniation, ipsilateral CN3 palsy and contralateral cerebral peduncle compression.
ICP management: IV acyclovir (if suspect viral), elevate head, optimize BP and ventilation, seizure control, IV mannitol, consult neurosurg
An old gentleman presented with tremor that is worse when watching TV, slowing of movement
PE: tremors worsen when he puts his hand on his lap, persistent glabellar tap
1. Most likely dx
2. 4 core features for dx
3. Name 2 classes of drugs that would worsen his symptoms+ cognitive functions
4. Name 2 common ddx for cause
- Parkinsons disease
- Tremor, rigidity, bradykinesia, postural instability
- Anticholinergics, sedatives. 1st gen antipsychotic, antiepileptic, antiemetic, L-dopa
- Multiple system atrophy, Lewy body dementia, Drug induced Parkinsonism, Vascular parkinsonism
A young woman works in the restaurant had a sore throat 2 weeks ago. She developed pins and needle numbness first at feet then at fingers and hands. Lower limbs weakness the morning of admission. Physical examination revealed hyporeflexia of upper limb, lower limb knee jerk and ankle jerk absent. Upper limb normal power, lower limb 4/5 power. ?Mild loss of pin-prick sensation over limbs
1. What is the most likely diagnosis
2. What Ix to do?
3. Describe Mx and 2 mx issues
- GBS/AIDP
- LP for protein, glucose, cell count and differential for albuminocytologic dissociation
Nerve conduction study: demyelinating pattern (low SNAP and CMAP in AIDP)
Nerve biopsy (differentiate axonal, inflammatory, demyelinating)
Antiganglioside antibodies: GM1b, GQ1b (Miller Fisher syndrome: opthalmoplegia) - Plasmapharesis/IVIG. High dose steroids to start off.
Autonomic involvement: monitor for dysphagia and respiratory function (FVC), spO2
Monitor cardiac function: arrhythmia, hypotenesion
Respiratory support and inotrope support and terminate arrhythmia
On steroid, Fever, headache, middle aged woman. CSF shows high protein, lymphocytosis, low glucose.
1. most likely dx
2. 2 diagnostic tests to confirm dx
3. 2 complications
- Acute TB meningitis
- CSF culture for AFB, TB PCR. Indian ink, fungal PCR to rule out fungal cause
- Acute hydrocephalus (basal meninges adhesion preventing reabsorption of CSF), cerebral infarction (tuberculous arteritis: MCA), CN palsies (3,4,6,7,8), tuberculoma, tuberculous brain abscess
a) Left ischemic stroke affecting the MCA
b) Yes it is within 4.5 hours of onset of symptoms
c) BP measurement (optimize), random blood glucose (optimize)
a) acute tuberculous meningitis
b) culture (ziehl neelson stain), TB PCR
c) hydrocephalus, cerebral infarction, CN palsies (CN 3,4,6,8), tuberculous brain abscess
a) Residual hemiparesis causing uncoordination between leg power.
Parkinsonism features caused by haloperidol (antipsychotic): rigidity, bradykinesia tremor –> susceptible to falls
Oxybutynin is a anticholinesterase (overactive bladder): AE is blurred vision (visual impairment easy to lose balance)
Prochloperazine (dopamine antagonist) used as an antiemetic: produces extrapyramidal symptoms (TRAP), orthostatic hypotension (prone to vasovagal syncope) resulting in falls
b) timed up and go test: patient rises from an arm chair, walks 3m, turns and walks back and sits down again w/o assistance. <10s is normal, >14s increased fall risk, >30s: dependent for ADLs
c) Ondansetron, Dexamethasone (both not dopamine blockers)
a. What is the main difference between MCI and mild Alzheimer’s disease?
b. Name 1 drug for mild AD approved by the FDA for Alzheimer’s disease. (1) What is the mechanism?
c. Apart from memory, list two cognitive domains that would be affected in AD.
d. Describe 2 side effects from 2 organ systems
e. Name 1 drug approved by the FDA for moderate to severe AD. (1) What is the mechanism?
a. +/-ADL
b. Rivastigmine: AChE bocker
c. Orientation, attention, language, executive function
d.
e. Memantine: NMDA antagonist
A patient was admitted for emergency surgery at night for sigmoid volvulus. He woke up at 11pm after surgery but with dense right sided hemiplegia. Urgent CT brain at midnight showed dense MCA sign.
a. Can you give IV thrombolysis? Why or why not?
His son is a high court lawyer and demands that you perform urgent reperfusion for him.
b. Are there any other revascularization methods? If no, why not? If yes, what is it and what investigation will you do beforehand
The patient was shown to have transient AF, hyperlipidemia and hyperglycemia.
c. Which of the above conditions predisposed to his stroke?
The patient regains some neurological function and you are discussing pharmacological methods to prevent recurrence of stroke
d. After revascularization, will you give antiplatelet or anticoagulant? Name some examples of the antithrombotic drugs you chose
a. No as he woke up with stroke features so is not definite what time was onset of symptoms (time window for tPA may have passed) + recent major surgery
b. Surgical embolectomy, DSA, coagulation profile
c. AF
d. Anticoagulants: DOAC (dabigatran, edoxaban, rivaroxaban)
A young 20+ year old lady presents with her mother. Her mother describes several episodes of her staring into the distance with focal twitching of the right upper limb. This lasts for several minutes until the patient returns to her normal state. The patient cannot recall the episode, and only recalls feeling slightly dizzy. She has no history of head injury or trauma. She has no focal neurological signs, fever or neck stiffness.
a. What is the clinical diagnosis?
b. What immediate investigations will you perform? Give 3
The patient is sent home after the investigations and is awaiting the results. However, presents again with generalized stiffening, followed by loss of consciousness and generalized convulsions.
c. What is the diagnosis?
d. What drug can you give to prevent the condition happening again?
a. Complex partial seizure. Focal onset, impaired awareness, motor onset seizure
b. EEG, CT brain, serum glucose
c. Complex seizure (partial seizure –> generalized tonic clonic seizure)
d. Valproate
A 25-year-old man with good past health collapsed suddenly after complaining of acute onset, un- precipitated severe headache referred to his occipital and neck regions. He was found to have neck stiff- ness and he was afebrile. He could open his eyes with pain, and localized the source of painful stimuli by withdrawing his limbs to pain. He could only make incomprehensible sounds.
(a) What is the most likely diagnosis?
(b) What is the Glasgow coma scale score by its components?
(c) Name three investigations that would be helpful to confirm this condition.
(a) SAH
(b) E2V2M5 (can localize pain)
(C) NECT for acute blood in sulci/star sign, CTA for aneurysm (spontaneous SAH), LP for blood/xanthochromia
An otherwise healthy 25-year-old secretary consulted you for episodic unilateral throbbing headaches. She started to experience on and off headaches when she was 15 years old. The headaches were infre- quent and less severe in the past, and relief was obtained by the use of simple analgesics. Following a recent chance in her job, her headaches have become more frequent, longer-lasting, more severe, and non-responsive to simple analgesics. Her general physical and neurological examinations are normal.
(a) What is the diagnosis of her headaches?
(b) Does she need a computed tomography or magnetic resonance imaging of her brain?
(c) What treatment can be offered to abort the headache?
(d) What treatment can be offered to reduce the frequency and severity of the headache?
(a) migraine without aura
(b) No. Characteristic of headache for migraine. Neuroimaging is reserved for those whose dx is in doubt or a/w focal neurologiacal features
(c) for severe migriane not responsive to simple analgesic,s D2 blocking antiemetics (maxolon) and triptans (sumatriptan) can be used
(d) prophylactic tx can be head BP
Antihypertensives e.g. verapamil
AED e.g. topiramate, valproate
Prophylactic use of analgesic with trigger e.g. stress, menstruation
Antidepressant e.g. amitryptyline, venlaxafine
Pizotifin
A previously healthy 20-year-old right-handed truck driver collapsed suddenly and was found to have a GCS score of 12 and right-sided neurological deficits. Urgent plain CT brain revealed a hyperdense lesion of about 6 cm in diameter and height over the left basal ganglia with moderate mass effect.
(a) What is the precise neurological diagnosis?
(b) What neurological deficits may be present?
(c) What are the potential complications in the acute and subacute stages?
(d) What are the possible underlying causes or predisposing factors?
(a) left basal ganglia hemorrhage with mass effect
(b) may affect left internal capsule (right hemiplegia +/-sensory loss)
left basal ganglia: right parkinsonism (unlikely in acute phase)
left thalamus: right hemisensory loss
Increased ICP: bilateral 6th nerve palsy
(c)
Acute:
Neurological: increased ICP with transtentorial or even tonsillar herniation –> coma and death
Systemic: immobilization related (bed sores, DVT, AROU), infection (UTI, pneumonia), metabolic
Subacute
Neurological: residual neurological deficits, post stroke epilepsy
Systemic: musculoskeletal (contractures, shoulder subluxation)
(d) bleeding tendency. HTN. vascular malformation, tumor
(a) pneumonia (CAP or aspiration), MG crisis triggered by respiratory infection
(b) pneumonia: consolidation signs (creps, bronchial breathing), lung consolidation on CXR. MGF crisis: generalized muscle weakness, reduced FVC but normral CXR, T2RF pattern on ABG (increased pCO2, normal O2), normal A-a gradient
(c) pyogenic bacteria: s. pneumoniae, mycoplasma pneumonia, klebsiella pneumoniae, viridans streptococci
TB: chronic steroid use
Viral: may just be URTI due to flu
(d) T2RF with respiratory acidosis. High pCo2 suggestive of hypoventilation, suggests MG crisis.