Neurology notes Flashcards
What information does the internal capsule transmit?
What is the consequence of stroke affecting this area?
What is blood supply?
Anterior limb: between the lentiform nucleus and caudate nucleus
Posterior limb: between the thalamus and the lentiform nucleus
* Contains fibers of the corticospinal tract and corticobulbar tract (face and UL)
* Posterior 1/3 of posterior limb: 3rd order sensory neurons from posterolateral nucleus of thalamus to the postcentral gyrus. Fibers of optic radiation from lower visual centers to the cortex of the occipital lobe. Acoustic fibers from the lateral lemniscus to the temporal lobe. Fibers that pass from the occipital and temporal lobes to the pontine nuclei.
Superior parts of both anterior and posterior limbs and the genu of hte internal capsule are supplied by the lenticulostriate arteries (branches of the M1 segment of the middle cerebral artery)
Pure contralateral hemiparesis.
What is the ddx of hyperthermic syndromes and treatment?
What is the SS and management of serotonergic syndrome?
What is the use of nerve conduction study?
- Demyelinating vs axonal neuropathy: decreased velocity in demyelinating, decreased amplitude in axonal
- Evaluting plexopathy/radiculopathy: F wave study
- Confirm entrapment neuropathy: presence of conduction block
How to evaluate NMJ lesions?
Repetitive nerve stimulation study
MG: >10% decrement at 3hz
LEMS: progressive increment at 20-50Hz (tetanic)
Use of somatosensory evoked potentials?
Principle: stimuli delivered to median, ulnar or posterior tibial nerves. Record waveform over plexus, spine and scalp
Utility
* Central conduction time: conduction time from dorsal column to parietal cortex. increased CCT –> spinal cord lesions e.g. MS, syringomyelia
* Giant SSEP –> characteristic of certain myoclonic disorders
* Intraop SSEP monitoring in spinal surgery
Parameters of CSF analysis
Opening pressure. Normal = 8-12cmH2O
- Appearance: blood (3 tube test if susect traumatic tap: if traumatic tap 3 tubes will significantly reduce in RBC. If actual RBC actual blood stained will be consistently stained), xanthochromia, turbidity
- Microscopy: cell count, WBC DC
- Biochemistry: protein, glucose (with serum glucose)
- Cytology: CNS malignancies
- Micbio: bacterial workup (gram smear, C/ST), TB workup (AFP smear, culture), fungal workup (indian ink smear, cryptococcal antigen test), serology for viral Ab, PCR for HSV DNA, TB DNA, cryptococcal DNA
- GBS: increased CSF protein with no pleocytosis
- Collagen vascular diseases (e.g. SLE, bechets disease): increased CSF protein with lymphocytosis
- Multiple sclerosis: increased CSF protein with lymphocytosis
- Xanthochromasia: SAH, increased SAD protein, jaundice
Dsyarthria vs dysphasia
- Dysarthria due to incoordiation of speech muscles
- Dysphasia due to involvement of Brocas or wernickes area or radiation
How to assess severity of stroke?
What types of strokes are there?
- NIHSS scale
- TOAST classification: cardioembolic, smell vessel disease, large artery atherosclerosis, stroke of other etiology, stroke of undermined etiology
How would a CXR suggest tb?
- Hilar lymphadenopathy
- Small nodules or patchy infiltration
- Cavitation
- Calcified nodules
- Apical fibrosis
- Pleural effusion
- Tuberculoma
- Miliary shadowing (diffuse reticulonodular infiltrate distributed fairly uniformly throughout both lungs
How to confirm TB meningitis?
- CSF AFB smear and culture
- CSF analysis by LP: raised WCC (lymphocyte predominant), raised protein, low glucose (<50% of blood glucose)
TBM is a medical emergency and treatment started which also covers bacterial or viral meningitis with ceftriaxone (gram-ve and +ve) + vancomyin (gram+ve) and acyclovir.
Other than increased ICP in meningitis what other complications are there?
- Granuloma formation in TBM
- Compression on CN may cause CN palsy presenting as diplopia, dysphagia or dysarthria
- Compression on ventricular system causing obstructive hydrocephalus. Can even cause coning (brainstem getting pushed down foramen magnum due to increased iCP)
- Arteritis and thus stroke presenting as hemiplegia, facial weakness or more specific neurologic signs depending on lobes affected
- Granuloma may serve as foci of irritation and cause seizure
- It can affect the spinal cord and cause myelitis if spread along meningies
- Spinal cord compression if abscess formation near spine
If posterior compression then DLCM i.e. propioception, vibration. If lateral compression than spinothalamic (pain and temp). If anterior compression –> motor loss.
Isoniazid causes peripheral neuropathy, what to give in advance to prevent SE?
Vit B6
2nd line TB drugs
- Kanamycin, amikacin
- Levofloxacin, ofloxacin
- Cycloserine
Why look for gaze and nystagmus in suspected Parkinsons disease case?
Not seen in PD
But seen in other parkinsonian syndromes e.g. progressive supranuclear palsy
What Ix to do in suspected rhabdomyolysis and Tx?
Creatine kinase (CK), LDH, RFT, CaPO4, urate, clotting profile and dimer and fibrinogen, urine dipstix and microscopy)
Appearance of urine (cocacola)
Correct hypovolemic (fluid enters injured muscle) and prevent proximal tubular toxicity from myoglobin deposition and clear heme protein
Check ECG (hyperK)
Monitor vitals and I/O
Resuscitation
Fluid resuscitation: 1-1.5L/hr continued until BP normalizes
Thereafter, continuve IV infusion with 500ml NS alternating with D5 1L/hour
Add NaHCO3- 50mmol/L to each 2nd or 3rd botle of D5 to keep urinary pH>6.5
Furosemide if volume overload from fluid infusion.
Dialysis for established acute kidney injury
Allopurinol if uric acid level >476 umol/L
Classes of anti-parkinsonism drugs
- L-dopa which increases dopamine synthesis
- Peripheral DOPA decarboxylase inhibitors: carbidopa (sinemet = Ldopa + carbidopa)
- NMDA antagonists: amantadine
- Anticholinergics
- MAOI class B: selegiline (decreased metabolism of dopamine in periphery)
- Dopamine agonists: bromocriptine
MoA of Ldopa, AE on both CNS and systemic
Ldopa is a dopamine precursor, converted to dopamine via the action of a naturally occuring enzyme called DOPA decarboxylase. This occurs both in the peripheral circulation and in the CNS after L-dopa has crossed the BBB
AE: postural hypotension, psychiatric (confusion, agitation, hallucinations), motor complications (dyskinesia)
What is bilateral innveration of facial nerve?
UMN lesion: upper face is spared due to bilateral innervation, only lower face on the contralateral side is affected
LMN lesion: whole ipsilateral face is affected
What signs to expect in a brainstem lesion?
Midbrain: CN 3-4 palsy, contralateral UMN hemiparesis
Pons: CN 5-8 palsy, contralateral Umn hemiparesis, cerebellar signs
Medulla: CN 5, 9-12 palsy, contralateral UMN hemiparesis, cerebellar signs
How to differentiate ICH is caused by arterial causes (e.g. hypertension) or venous thrombosis?
- Venous thrombosis should be considered in the assessment of confluent infarct or hemorrhage in atypical; areas, crossing arterial territories or infarcts with cortical sparing
- These are structures typically seen in parasaggital structures (following saggital sinus thrombosis) temporoparietal regions (transverse/sigmoid sinus thrombi( or dee pstructures.
- Mainly differentiated by the distribution of hemorrhage: venous hemorrhage crosses arterial territories
Superficial –> superior saggital sinus
Deep –> transverse, straight and sigmoid sinuses
Inferior saggital sinus and great cerebral vein joints into straight sinus
Superior saggital sinus, straight sinus and occipital sinuses joint at the confluence of sinuses than branch into transverse sinus which then become sigmoid sinus.
Sigmoid joins into inferior petrosal vein into internal jugular vein
How to manage patients with cerebral venous thrombosis?
Acute
* NCCT
* Monitor vitals, GCS, neurological signs, raised ICP signs
* LMWH - to recanalize the thrombosed vein
* Measures to control and monitor ICP
* Treat any seizures
Long term
* Workup for underlying cause of thrombophilia
* Long term warfarin (2-7% rate of recurrence without long term anticoagulation)
* Rehabilitation if venous stroke occurred
What ix to dx neuromyelitis optica?
- MRI brain and spinal cord: NMO has a predilection for spinal cord and optic nerve. Optic neuritis is still more commonly unilateral like MS, but if its bilateral or closely sequential then it suggests NMO –> MS
- Thus, the brain is usually spared during the initial presentation, in contrast to MS where it is commonly involved
- Serology: Anti AQP4 Ab, MOG Ab (myelin oligodendrocyet glycoprotein)
- CSF: elevated WCC (PMN predominates), protein, oligoclonal bands in minority
How to diagnose multiple sclerosis?
MS requires dissemination in space and dissemination time (DIT)
Each of these can be demonstrated clinically or radiologically
Dissemination in space: 2 attacks in affecting 2 separate areas; or 2 plaques identified on MRI
Dissemination in time (DIT): 2 clinical attacks or the coexistnce of gadolinium enhancing (new) and contrast non enhancing (old) plaques on MRI or the presence of CSF specific oligoclonal bands of IgG
Clinical features of multiple sclerosis
- Optic neuritis: typically unilateral. Impaired vision
- Internuclear opthalmoplegia as a result of lesion in the medial longitudinal fasciculus. Ipsilateral medial rectus weakness but an intact convergence reflex
- Demyelination of spinal cord tracts. Lhermitte sign: shotting electric sensation that travels down the spine upon flexion of the neck. Pyramidal tract lesion: UMN weakness, spasticity, hyperreflexia. DCML: loss of vibration and fine touch sensation
- Cerebellar involvement: poor postural control, imbalance, gait dysfunction. Charcot neurological triad: scanning speech, nystagmus and intention tremor
- Tranverse myelitis: asymmetric paraplegia, unilateral sensory loss, bladder dysfunction
- CN palsies: diplopia, facial palsy and trigmeinal neurlagia
- Autonomic dysfunction: bowel and bladder neurogenic disorders (urinary incontinence)
What CT findings of MS?
Where are the lesions normally found?
CT findings: homogenous hypoattenuation, non specific changes
McDonalds criteria for lesion location: juxtacortical, periventricular, infratentorial and spinal cord regions
In MS how does it affect the optic nerve?
3 types of optic neuritis
* Most common is MS is retrobulbar neuritis: normal optic disc
* Papillitis: hyperemic and edematous optic disc, with peripapillary flame shaped hemorrhages (most common in children)
* Neuroretinitis (least common): macula star (swelling of optic disc and macula)
In optic neuritis suspected MS what further Ix to do?
- MRI orbit
- Visual evoked response potential test (delayed response)
Immunosuppressant used in multiple sclerosis
What IFN used in MS?
How does IFN work in MS?
- Glatiramer acetate, mitoxantrone
- Fingolimod, natalizumab, alemtuzumab
- IFN beta 1a/1b
- Antiinflammatory: prevent T cell activation and proliferation, induce apoptosis of autoreactive T cells
Causes of cerebellar ataxia
- Acute: vascular (infarct, hemorrhage), alcohol and drugs (anticonvulsants, barbiturates, chemotherapy), infections (EBV, VZV, Lymes disease, tertiary syphilis, malaria)
- Subacute: demyelination (MS, ADEM, Miller Fisher syndorme, alcoholic cerebellar degeneration, malignancy, endocrine, nutritional (B1 (wernickes encephalopathy), B12 deficiency)
- Chronic: hereditary (SCA, TA, FA, WD, Arnold-Chiari malformation)
How to differentiate dizziness, syncope and vertigo?
- Dizziness: whirling sensation with tendency to fall, confusion
- Syncope: transient loss of consiousness
- Vertigo: spinning sensation, false sensation of motion
Central and peripheral causes of vertigo?
- Central: brainstem/cerebellar/vertebrobasilar stroke/cerebellopontine angle tumor
- Peripheral: BPPV, Menieres disease, vestibular neuritis, ramsay hunt syndrome, aminoglycoside toxicity
What other sites will you look for in ramsay hunt syndrome?
Ramsay hunt syndrome
* Triad of ear pain, ear vesicles, facial nerve palsy, may have ipsilateral altered taste sensation and lacrimation
* Can also spread to CN8 (tinnitis, vertigo)
* Rarely involves CN5,9,10
Herpes zoster ophtalmicus
* V1 distribution rash and pain
* Conjunctivitis, uveitis, keratitis (can cause visual loss)
How to manage MG?
If MG patient presents with marked weakness and fatigbility to you what to suspect?
- Mestinon: pyridostigmine –> anticholinesterase –> inhibits action of cholinesterase –> so more ACh available for neuromuscular transmission
- If doesnt respond –> give moderate to high dose steroids
- Try immunosuprpessant: azathioprine
- Give IVIG for approx 3 weeks
Suspect myasthenic crisis. If taken more than required pyridostigmine –> cholinergic crisis
Cerebellar syndrome causes?
Approach to generalized weakness
Cause and features of acute axonal vs chronic axonal polyneuropathy
Cause and features of acute vs chronic demyelinating polyneuropathy
SS of polyneuropathy and clinical approach?
considerations of ddx for polyneuropathies?
Workup for polyneuropathy if severe and no clear cause (DM neuropathy)?
Mx for polyneuropathy?
What are the types of GBS?
Clinical features of GBS?
Ix for GBS
ddx for GBS
Mx of GBS
Characteristics of miller fisher syndrome in comparison to GBS
Clinical features, Ix, ddx and Mx for CIDP
Causes of hereditary motor and sensory neuropathy?
SS?
Ix?
Charcot marie Tooth disease
Hereditary neuropathy with liability to pressure palsies
Anterior horn cell disease in paeds, gene involved?
Classification?
Ix and Mx
Clinical presentation of motor neuron disease
□ Characteristically mixed UMN + LMN signs sparing ocular and sphincters
□ No autonomic or sensory losses
Causes of toxic neuropathies and clinical presentation
Inherited and acquired causes of myopathies?
Causes featrures and SS of myotonic dystrophy?
Pathogenesis of periodic paralysis
What are the subtypes:
□ Characterized by episodic generalized flaccid weakness of varying severity
→ Usually spares respiratory and bulbar muscles
→ Lasts 10min to several hours
Ix for inflammatory myopathy?
