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.
(a) GTCS + SIADH due to viral encephalitis
(b) send CSF for PCR (HSV, VZV, EV) and viral culture
CSF TB PCR, AFB smear/culture, cryptococal antigen, indian ink smear
CSF gram stain C/ST
Blood for JEV IgM, blood C/ST
Urine feces, throat swab for viral culture
(c) IV acyclovir +/- meningitic cover (ceftriaxone, vancomycin)
(d) HSV, VZV
A 26-year-old lady was seen in outpatient clinic complaining a 2-month history of intermittent double vision with drooping of her left eyelid, worse when looking to her left. She did not have any pain, fever or headaches, and had no previous significant medical history. She was not on any medication. She has no dysarthria, dysphagia, sensory or urinary symptoms. Her symptoms appear to be worse in the evening. On examination, the pupils were symmetrical in size, and there was mild left partial ptosis with mild dysconjugate eye movements, affecting her left eye, when she tried to look to her left.
(a) What is your most likely diagnosis?
(b) What clinical bedside test would help you confirm your diagnosis?
(c) What other tests would you use to support your diagnosis?
(a) ocular MG
(b) tensilon test (2-3 min), sleep test (30 min), ice pack test (2-3 mi)
IV edronophium improves ptosis in 2-3 min (more ACh available)
(c) EMG for RNS >10% decrement in 3Hz repetitive stimulation
Anti AChR and antiMuSK
CT thorax for thymoma, TFT for associated thyroid disorder (young onset), ANA, anti-ENA, RF
A 28-year-old woman with good past health complained of one-month history of painless mild double vision & drooping of her left eye lid which is worse in the late afternoon, when compared to the morn- ing. This was associated with mild weakness of her both upper and lower limbs such that she found it more difficult to comb her hair or climb up stairs. There is no sensory disturbance, although she claims that she is more breathless on exertion. Her family also noticed that her speech was slurred in the evenings. She was not on any medication and has no family history. She has no urinary or bowel symp- toms. On examination, there was mild left partial ptosis and diplopia on looking to her left, which worsened with prolonged upward gaze. Her proximal limb power appeared weaker than her distal limb muscles and the limb reflexes were normal. There was slight dysarthria when she was asked to read aloud over a prolonged period.
(a) What is the most likely diagnosis?
(b) What investigations would be helpful to support or confirm your diagnosis?
(c) What other disorders are associated with her illness?
(d) What likely drug treatment options would you use to treat her illness?
(a) generalized MG
ddx:
myopathies: metabolic (endocrine (thyrotoxicosis, hypothyroidism), mitochondrial encephalopathy)
Myasthenic syndrome (lambert eaton syndrome), less likely because eye muscles usually spared in myasthenic syndrome and symptoms improve with ms use
(b) tensilon test (using edrophonium (AChR inhibitor), NPS (repetitive nerve stimulation showing decrement in amplitude of 4th and 5th muscle action potential), sleep test, ice pack test
Others: CT thorax (thymic enlargement), CK (exclude muscle disease), TFT (dysthyroid eye disease and for concomitant thyroid disorders), autoantibodies (ANA, RF, anti thryoid antibodies to detect associated autoimmune conditions)
(c) young onset MG is a/w organ specific autoimmune disease
MG is also a/w thymic pathologies e.g. thymoma (10%) and thymic follicular hyperplasia (70%). Others: autoimmune thyroiditis, autoimmune adrenalitis, DM, RA, IBD etc
(d) 1st line = cholinesterase inhibitor usually pyridostigmine (mestinon) for its longer duration of action (4h)
If inadequate than start immunosuppression with steroids, subsequently tapering for steroid sparing tx (azathioprine, cyclosporineA)
If a/w thymoma or generalized MG + risk < benefit –> consider thymectomy
A 20-year-old undergraduate had fever, headache and vomiting for 6 days. Physical examination was normal. Urgent computed tomography of the brain was unremarkable. Lumbar puncture revealed a total cell count of 100 × 106/L (50% lymphocytes and 35% neutrophils), CSF protein of 1.6 g/L, CSF glucose of 2.5 mmol/L (simultaneous blood glucose was 6.4 mmol/L), and CSF Gram smear was nega- tive.
(a) What are your differential diagnoses?
(b) What additional tests on CSF are useful?
(c) Please outline your management.
(a) meningitis (bacterial), TB, cryptococcal, aspetic (SLE, carcinoma)
(b) CSF C/ST, TB PCR, AFB smear/culture, Indian ink smear, cryptococal antigen
(c) ensure ABX
Neuroobs Q4h
Blood Ix
IV access for fluid rehydration
Urgent IV acyclovir, meningitic dose of ceftriaxone/vancomycin
Watch out for Cx e.g. increased ICP, seizure and manage accordingly
Consider further imaging e,g, contrast CT/MRI to r/o any SOL
A 63-year-old woman had a slow car crash into a supermarket car park concrete wall. Three witnesses observed her to be unconscious at the wheel before the crash and she recovered consciousness some seconds after they approached the car an opened the door. She was briefly confused, but left soon after with a friend. She consults you next day about this incident.
(a) What is the differential diagnosis for her collapse?
(b) What investigations should be performed?
(c) What other management should you initiate?
(a) Neurology: seizure with post ictal confusion, TIA
Cardiac: syncope,
Systemic: anemia, hypoglycemia
Psych: psychogenic
(b) CBC (Hb for anemia), RFT (electrolytes), hstix, urgent NECT (rule out intracerebral hemorrhage), ECG, holter (underlying clot formation), EEG, consider MRI
(c) stop driving, workup
You are called to see a previously well 20-year-old student who has presented to the Accident and Emergency Department with a 24-hour history of increasing headache and myalgia. On examination there is definite neck stiffness and a temperature of 39°C. The neurological examination is otherwise normal, as are the optic fundi. You suspect there are conjunctival petechiae.
(a) What differential diagnosis would you consider?
(b) What immediate investigations would initiate, and would you start any treatment?
Later results from examination of the cerebrospinal fluid show 800 neutrophils/μl, with a CSF glucose 1.7 mM/L (blood glucose 5.6 mM/L), and the Gram stain shows Gram negative intracellular diplococ- ci. You learn two other students have been admitted with an identical illness.
(c) What is now the diagnosis, and what potential complications may occur?
(d) What further action can be taken to protect the student’s roommates and to prevent further
cases in the institution? Can such action fully protect against this disease?
(a) pyogenic meningitis (meningococcus or pneumococcus) as evidenced by acute onset of increasing headahce with neck rigidity, conjunctival petechiae and systemic features such as myalgia, and dever
petechiae on trunk, legs conjunctiva are classic for neisseria meningitis
Other ddx:
infection: systemic infection (meningitism), encephalitis, brain abscess
substance abuse/drug intoxication
b) septic workup (throat and nasal swabs, sputum, blood, CSF)
CBC, ESR, clotting profile, L/RFT
LP for CSF analysis
Urine toxicology screen (potential substance abuse)
(c) meningococcal meningitis as evidenced by CSF analysis of elevated neutrophils, low glucose and gram negative intracellular diplococci and clinically supported by conjunctival petechiae,
Potential complications: local spread of infection (cerebritis, cerebral abscess, subdural effusion), meningeal adhesion: obstructive hydrocephalus, increased ICP, CN palsies), arteritis or thrombophlebitis (cerebral infarction), seizure and epilepsy. Waterhouse friderichsen syndrome (fulminant meningococcemia): septic shock, bilateral hemorrhage into adrenal glands and adrenal insufficiency, abrupt onset of hypotension and tachcyardia, rapidly enlarging petechial skin lesions
(d) contact tracing and chemoprophylaxis: rifampicin or fluoroquinolone prophylaxis for close contacts.
A 31-year-old secretary had diplopia and drooping of her eyelids for 4 weeks. Her symptoms worsened after reading or watching television and much improved after sleep or rest. She did not have any prob- lem with her speech, swallowing, breathing sensations or urinary and bowel functions. She has a past history of peptic ulcer, thyroid disease and vitiligo. Her family history is positive for pulmonary tuber- culosis, chronic obstructive pulmonary disease, hypertension, diabetes mellitus and ischaemic heart dis- ease. Three days before admission, she started to have fever, cough and sputum. These symptoms were improved after taking the medications from a general practitioner. On the day of admission, her diplop- ia and drooping of eyelids became much worse. In addition, she had generalized weakness with dysarthria, dysphagia and breathlessness.
(a) What are the differential diagnoses for diplopia plus dropping of the eyelid?
(b) What is the most likely diagnosis for her diplopia plus drooping of the eyelid?
(c) What tests are useful in confirming the most likely diagnosis of question (b)?
(d) What are the related diseases/problems in her past health and family history?
(e) What should be the working neurological diagnosis during her admission?
(f) Please outline the management principles for the neurological diagnosis of question (e).
(a) MG, CN3 palsy
Other less likely ddx
Myopathies. Metabolic (endocrine: thyrotoxicosis, hypothyroidism), mitochondral encephalopathy), polymyositis
Myasthenic syndrome (eaton lambert syndrome) less likely because eye muscles usu spared.
Dysthyroid eye disease, unlikely because no drooping in dysthyroid eye disease
(b) Generalized MG with MG crisis precipitated by respiratory infection
(c) tensilon test, sleep test, ice pack test
(d) thyroid eye disease, vitiligo –> organ specific A/I disease is a/w early onset MG
PUD –> Steroid may be used, therefore need PPI prophylaxis
FHx of pTB –> must screen well for latent TB before starting steroid
FHx of HT, DM, IHD –> steroid has metabolic concerns, should consider early steroid sparing therapy
(e) Generalized MG with crisis
(f) treat underlying cause
Optimize respiration: prop up, clear airway, give O2
Monitor swallowing/FVC. Ventilate if FVC < 15ml/kf or T2RF or cannot protect airway
Start prednisolone 1mg/kg/d
IVIG or plasmapharesis
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