Neuro Flashcards
Myasthenic crisis
HB
Definition: Severe generalized weakness and need for RS
support.
*Tensilon test - diagnostic test in untreated disease; not
reliable in differentiating myasthenic and cholinergic crisis and
not without risk, hence not recommended.
Mx
1. Watch out for RS failure in any patient with
progressive weakness and bulbar Sx
- Closely monitor FVC, SaO2 ± ABG
- General supportive measures and ICU care
- Intubate and initiate mechanical ventilation if FVC < 15-20
ml/kg, hypercarbia, hypoxia or patient exhausted - Stop anticholinesterase if patient is intubated
6. Give IVIG 0.4 g/kg/day for 5 days. An alternative is plasma exchange 50 ml/kg daily or on alternate days until adequate response achieved (usually after 5 - 6 exchanges)
- Resume anticholinesterase at a smaller dose 48-72 hours after
stabilization and titrate according to response - Start prednisolone 1 mg/kg/day; beware that early
steroid-induced deterioration may occur - Identify and treat any precipitating conditions (e.g. underlying
infection) - Be cautious with the use of any drug that might worsen MG.
e.g. Aminoglycosides, quinine, quinidine, procainamide,
BB, muscle relaxants, penicillamine, Mg
Stroke Mx
HB
- Admit to designated acute stroke unit.
- Initial assessment: vital signs including airway, respiration,
hemodynamics, conscious level and neurological impairment. - Ix : Urgent NCCT brain, CBC, R/LFT, PT, aPTT,
blood glucose, lipid, CXR, ECG. - Special Ix (in selected cases): MRI, MRA, CTA, Echocardiography, Duplex carotid a, Transcranial Doppler cerebral angiography, hyper-coagulopathy assessment and AI screening.
- Supportive Mx
a) Regular monitoring of neurological and vital signs
b) Swallowing assessment before feeding, positioning ± splinting to avoid aspiration, contractures, pressure nerve palsy, shoulder subluxation, pressure sores, etc
c) Ensure good hydration, nutrition and oxygenation
d) Meticulous control of blood sugar and pyrexia
e) Cautious and gradual lowering of elevated BP
- In ischaemic stroke, lowering of BP is considered:
♦ in case of HT emergencies (eg: hypertensive
encephalopathy, aortic dissection, ARF,
APO or AMI)
♦ when systolic >220, or
diastolic >120, according to
repeated measurements 20 mins apart.
♦ when thrombolytic therapy is considered/given - In hemorrhagic stroke, lowering of BP is
considered:
♦ if systolic >200 or the mean BP >150
♦ if systolic >180 or the mean BP >130 when there is no clinical evidence of elevated ICP
f) Seizure should be treated promptly but prophylactic
anticonvulsant is not indicated for ischaemic or hemorrhagic stroke.
g) Early allied health therapists’ referral and assessment.
Specific therapy for Ischemic stroke
HB
a) Aspirin within 24-48 h onset. Withhold for the
first 24 hrs if given thrombolytic
b) Thrombolytic therapy:
Indication:
♦ Ischemic stroke onset within 3-4.5 hr
♦ Good premorbid function
c) Immediate anticoagulation may be considered in:
- Arterial dissection
- Documented cardiac source of embolism
- Cerebral venous thrombosis
CI and precautions
- BP > 180/110 mmHg
- Large infarct
d) Decompressive Hemicraniectomy for malignant MCA
syndrome (massive MCA territory infarct with eye
deviation, dense hemiplegia and progressive drowsiness +/- unequal
pupil size. Serial CT will show significant infarct with swelling and midline shift).
ICH
HB
a) Urgent reversal if elevated INR due to warfarin:
♦ Give IV vitamin K1
♦ Give prothrombin complex concentrate (PCC) +/- FFP
♦ Give FFP ASAP if PCC is not available
b) Neurosurgical consultation if large, SAH, hydrocephalus
Secondary prevention of stroke
HB
- Risk factor modification
- Oral anticoagulation in cardioembolic stroke (including
non-valvular AF) and anti-phospholipid antibody syndrome - Aspirin daily for ischaemic stroke if anti-coagulation
not indicated.
Aspirin + controlled release dipyridamole or
clopidogrel are other options for first line anti-platelet agents.
Dual anti-platelet agents may be considered in very high risk - Carotid endarterectomy or carotid stenting is indicated for symptomatic extracranial carotid stenosis of 70-99%
Intervention for symptomatic stenosis of 50-69% can be considered.
Muscle power (wiki)
0: No visible/palpable contraction
1: Visible/Palpable contraction with no motion
2: Full ROM without gravity
3: Full ROM against gravity
4: Full ROM against gravity, moderate resistance
5: Full ROM against gravity, maximum resistance
UMN signs
- Spastic paralysis
- Little atrophy
- Hypereflexia
- Clonus
- Babinski sign
- Increased muscle tone
LMN signs
- Flaccid paralysis
- Early-onset atrophy
- Hyporeflexia
- Fasciculations
- Decreased muscle tone
Signs of lesion @
- Hemisphere
- Posterior cranial fossa
- Spinal cord
- Spinal root
- Plexus
- Peripheral nerve
- NMJ
- Muscle
- Hemisphere
- Impaired higher mental fx, dysphasia, dyspraxia運動困難, homonymous hemianopia, UMN type motor weakness - Posterior cranial fossa
- CN deficits, bilateral UMN type motor weakness, bilateral sensory deficits, cerebellar ataxia - Spinal cord
- UMN type below; LMN type at the level, dissociated sensory loss - Spinal root
- Segmental distribution of LMN type motor weakness, segmental sensory deficits - Plexus
- Multi-segmental distribution of LMN type motor weakness, multi-segmental sensory deficits - Peripheral nerve
- LMN type motor weakness / Sensory deficit in peripheral nerve distribution - NMJ
- Focal or generalized weakness with fatigue, normal or reduced tendon reflexes, normal sensations - Muscle (Myopathy)
- Proximal weakness (shoulder girdle, pelvic girdle), preserved tendon weakness, normal sensations
RF for stroke
Unmodifiable vs Modifiable
Non-modifiable
- Old age
- Male
- History of TIA or Stroke
- PVD (Peripheral vascular disease)
Modifiable
- HT
- Heart disease
- AF
- DM
- HL
- Smoking
- Alcohol
- Carotid stenosis
- OC pills
- High plasma fibrinogen
- High blood viscosity
- Obesity
- Lack of exercise
- Homocysteinemia
Neuromyelitis optica (aka Devic’s disease, NMO)
Simultaneous inflammation and demyelination of optic n. and spinal cord
Attacks myelin by AutoAbs (Unlike MS which is by T cells)
Miller Fisher syndrome
- Variant of GBS
- Ataxia, Areflexia, Ophthalmoplegia
- Additional: generalized muscle weakness, RS failure
- Ab: Antiganglioside Ab (↑GD1b; GBS: ↑GD1a and GM1)
- Main reason for admission should be ataxia (could also be diplopia)
Multiple sclerosis S/S
- Fatigue
- Optic neuritis (usu 1 eye)
- Acute transverse myelitis
- Diplopia by CN palsy / INO
- Cerebellar Sx
- Lhermitte sign: Shooting sensation from back to limbs, elicited by neck flexion (due to involvement of posterior columns)
- Depression
- Cognitive dysfunction
- Heat intolerance (Uhthoff’s phenomenon)
- Urinary sphincter dysfunction
- Trigeminal neuralgia
Multiple sclerosis types
Relapsing-remitting (85%)
Secondary progressive (50% of RRMS will become this in 10-15y)
Primary progressive
Progressing-relapsing
Domperidone for PD with nausea
@_@
Déjà vu
Feeling that the situation currently being experienced has already been experienced in the past
Asso w/ Temporal lobe epilepsy (MCQ)
Brown-Sequard syndrome (Unilateral transverse lesion)
- Loss of all sensation at the level
- Ipsilateral below level: UMN signs + Impaired proprioception and vibration
- Contralateral below level: Impaired pain and temp (Spared motor)
Causes
- Trauma (stab, bullet)
- Asymmetrical compression from tumor or spondylosis
- Radiation necrosis
Lateral medullary syndrome
aka Wallenberg syndrome
PICA affected
- Ipsilateral CN 5
- Contralateral loss of pain + temp below level (Spinothalamic tract)
- Ipsilateral paralysis of palatal + laryngeal muscles (Nucleus ambiguus, CN 9, 10) –> slurred speech, dysphagia
- Horner’s Syndrome
Cerebellum signs
Vermis
- Truncal ataxia
- Dysarthria 構音障礙 *Cerebellar speech: ↑Volume, different from Parkinson’s which is ↓volume
Cerebellar hemispheres
- Dysmetria辨距障礙 (past pointing, intention tremor: finger-nose test, heel-shin test)
- Dysdiadochokinesia (abnormal rapid repetitive movement)
- Dysarthria
- Rebound phenomenon
- Broad-based gait
- Nystagmus
Internuclear ophthalmoplegia
Injury to medial longitudinal fasciculus (MLF)
- a heavily myelinated tract that allows conjugate eye movement by connecting the paramedian pontine reticular formation (PPRF)-abducens nucleus complex of the contralateral side to the oculomotor nucleus of the ipsilateral side
Asso w/ Multiple sclerosis
UMN signs
- Spasticity
- Hypertonic
- Hyper-reflexia, Babinski sign
- Weakness
- Clonus
LMN signs
- Fasciculations
- Hypotonia
- Hyporeflexia
- Weakness
Sphincter disturbance cord level
L1-S5
UL spared, LMN in LL
Vit B12 deficiency cord problem
Subacute combined degeneration of cord
- Dissociated sensory loss (Posterior column affected)
(Spinothalamic spared)
