Neurology Flashcards
BENZO S/e
sedation resp depression Agitation ataxia sudden w/d - seizure tolerance
phenytoin s/e
HYPERPLASIA GIGIVAL Hirtuism decrease BMD decrease folic acid drownsiness rash nystagmus
Primidone
biotransformation into metabolites phenobarbitone and phenylethylmalonamide → anticonvulsant activity
Use: GP FEM generalisedseizures, psychomotor (temporal lobe) epilepsy, focal seizures, myoclonic jerks
Adverse effects: Decreased bone mineral density, ataxia, drowsiness, fatigue, hyperirritability, suicidal ideation, vertigo, rash, GI upset, impotence, haematological, nystagmus, diplopia
Comments: May reduce effectiveness of hormonal contraception
s/e CARBAMAZEPINE
hyponatraemia, rash, pruritus, fluid retention, aplastic anaemia, hepatotoxicity, GI effects, sedation, ataxia, nystagmus, depression, dizziness, diplopia, lethargy, headache, idiosyncratic
May make primary generalised epilepsy worse.
Valproate moa and s/e
inhibits na channel S/e - NTD - PCOS = hypothyroidism = insulin resistent DM
ETHOSUXAMIDE moa and s/e
nausea, vomiting, sleep disturbance, drowsiness, and hyperactivity
Comments: Rarely lupus-like reactions, SLE
MOA: iBlocks T-type calcium channels in thalamic neurons
lamotrigine s/e moa
Rash (Stevens-Johnson), tremor, headache, GI, insomnia, somnolence
moa blocks Na and decrease electrical emission
how is VIGABATRIN secreted
really
VIGABATRIN s/e
Sedation, fatigue, depression, psychosis,, headache, dizziness, weight gain
TOPIRAMATE s/e
Sedation, cognitive slowing, renal stones, weight loss, glaucoma, paresthesias, headache, fatigue, dizziness, depression, mood problems, metabolic acidosis
gabapentine moa and s/e
increase GABA in the brain binds to voltage dependent calcium channel
edation, dizziness, ataxia, GI upset, weight gain.
TIAGABINE moa and s/e
GABA uptake inhibitor
potential pro-convulsive effect
Dizziness, tiredness, mood changes, lack of energy, somnolence, nausea, nervousness, TREMOR , DIFFICULT CONCENTRATION , abdominal pain
ZONISAMIDE moa and s/e
blocks voltage-dependent sodium and T-type calcium channels
Somnolence, ataxia, cognitive slowing, weight loss, rash, ataxia, anorexia, confusion, abnormal thinking, nervousness, fatigue, and dizziness, nephrolithiasis (low risk)
what two anticonvulsants cause nephrolithiasis
ZONISAMIDE
TOPIRAMATE
LEVETIRACETAM moa s/e
Unclear, binds to a synaptic vesicle protein, may modulate synaptic transmission through alteration of vesicle fusion, may indirectly modulate GABA
Usually well tolerated
Sedation, mood disturbance, behavioural disturbance, fatigue, somnolence, dizziness, and infection (upper respiratory
what anticonvulsants mess the OCP effectiveness up
phenytoin
Primidone
Carbamazepine
lamotrigine
what three anticonvulsants are excreted renally vs. hepatic
- VIBigatrin
- Zonisamine
- Gabapentine
4/ levetiracetam
Ulnar nerve Supplies and defect if damage
C8 , T1 supplies All small muscles of hands except LOAF Wasting of small muscles of hand Claw hand Sensory loss over medial one and half fingers Froment’s sign
Radial nerve Supplies and defect if damage
C5-C8 Supplies Triceps Brachioradialis Extensors of hand Wrist drop Sensory loss over anatomical snuffbox
Median nerve
C6-T1 Supplies Muscles of forearm (except FCU, FDP) LOAF Sensory loss over palmar aspect of thumb and lateral two fingers Ochsner’s clasping test Tinel’s test Phalen’s test
Sciatic nerve
Supplies Hamstrings All muscles below knee Footdrop Weak knee flexion Normal knee jerk, absent/weak ankle jerk Sensory loss posterior thigh, lateral and posterior calf and foot
Common peritoneal nerve
L4-S1 Terminal branch of sciatic nerbe Supplies Anterior and lateral leg compartments Weak dorsiflexion/eversion Normal reflexes Sensory loss lateral dorsum of foot
Brown Squard Syndrome
IPSILATERAL - UMN sign below lesion, LMN at level of lesion and VIBRATION AND propioperception
CONTROLATERAL temp and pain
SACD spinal cord
Symmetrical UMN signs in lower limbs Exaggerated knee jerks Absent ankle jerks Symmetrical proprioception/vibration loss Peripheral neuropathy Optic atrophy
CAUSE OF SACD SPINAL CORD
B 12
SYRINGOMYELIA
A fluid-filled, gliosis-lined cavity within the spinal cord
Pain/temperature loss over neck/shoulders/arm (cape)
Arm atrophy
UMN lesions in LL
Causes
Congenital malformations (e.g. Chiari malformation Type 1)
Postinfectious
Postinflammatory (e.g. transverse myelitis, MS)
Posttraumatic
CONUS MEDULARIS
Lesions at vertebral level L2
flaccid paralysis of the bladder and rectum
impotence
saddle (S3-S5) anaesthesia, usually more localised to perianal area.
Causes
disc herniation
spinal fracture
Space occupying lesion
seizure
sudden change in behaviour or function due to neurological dysfunction
epilepsy - recurrent seizures (at least 2) due to excessive electrical activity in the brain
Complication of epilepsy
AAA CDD T AED S/e anorexia Acidosis Cognitive impairment Depression death Trauma / personal injury
Risk of epilepsy recurrence
- structural brain disease
- cognitive impairment
- multiple seizure type
- age onset in 1st decade ( 10 years)
- family history
- not responding to treatment
- combo treatment needed
- abnormal neuro exam
- epileptiform foci on EEG
- Abnormal MRI
Seizure biomarkers
CLP cortisol creatinine kinase LDL Prolactin Ph
provocation testing for seizures on EEG
- sleep deprivation
- hyperventilation
what classification is used for seizure
ILAE 2010
definition of MND
Progressive group of neurological conditions which affects motor neurons at the anterior horn cell. characterized by both UMN and LMN lesions and sensory invovlemt is unlikely
what does bulbar involvement mean
Means the medulla is affected and it involves CN 9-12
RESULTS IN : dysarthria, dysphasia and laryngospasm
pathogenesis of MND
Nerve damage and loss Both axonal and myelin damage Subsequent gliosis occurs Spinal cord atrophy Muscle atrophy Intracellular inclusions
Epidemiology of MND
2 types
- sporadic
- Familial - SOD1, TARDBP , CaORFT2
OLDER AGE
what are the additional symptoms you can get in MND
- Cognitive impairment - 3 types: 1. Pseudobulbar palsy
dementia and
frontal Temporal lob (executive function and memory - Autonomic dysfunction
- falls
- urinary retention - catheter - recurrent UTI
- constipation - bowl obstruction - Parkinsonian features
- Sensory - complain 20%, but no exam finding
UMN and LMN symp in MND
UMNL
- stiffness (HEAVY , Dragging)
- clonus
- spasm
LMNL
- weakness and atropin
fasciculation
cramps
UMN and LMN signs in MND
UMN Spasticity Slowed rapid alternating movements Increased reflexes Gait disorder Spastic
LMN Weakness Gait disorder Reduced reflexes Muscle atrophy and fasciculations
Distal spread UMNL
contraction of muscles that produce motions other than the one associated with the test muscle
Hoffman’s sign
tapping the nail or flicking the terminalphalanxof the middle or ring finger. A positive response is seen with flexion of the terminal phalanx of the thumb.
Crossed adduction
contraction of the adductors of the thigh and inward rotation of the limb elicited by tapping the sole.
Triple flexion
Flexion at the hip, knee, and ankle, in response to stimulation of the sole of the foot.
palmomental sign
stroke palm see twitching - bulbar uMN L
ALS pulse syndrome
Frontotemporal dementia, Autonomic dysfunction Parkinsonism Supranuclear gaze paresis Sensory loss
Ddx MND
- multifocal motor neuropathies
- multifocal myopathies (dermatomyositis, polymyositis)
- Hereditary neuropathies (hereditary spastic paralysis, spinobulbar muscular dystrophy)
- inflammatory neuropathies (incision body myositis)
Others:
post polio syndrome
paraneoplastic (ovaries, lung, renal)
Exclusion Criteria
Clinical or electrophysiological - suggest other condition (e.g.hx of poliomyelitis)
Neuroradiological evidence of a condition that could otherwise account for the clinical syndrome (e.g. evidence of cervical myelopathy)
Failure of the condition to progress
El escorital criteria
LMN degeneration by clinical, electrophysiological, or neuropathological examination
UMN degeneration by clinical examination
Progressive spread
investigation of MND
Electrophysiology (EMG) - fibrillation - positive sharp waves Nerve Conduction studies (do repetitive test to look for fatiguability) potential Imaging Blood and CSF analysis - HIV, Septic screen, serum cA2+, TFT, SPEP and LP MRI BRAIN
investigation for complication of MND
- RESPIRATORY FUNCTION
- MSU - infection
renal US - stone - full swallow assessment (video fluoroscopy)
- Constipation - PFA
treatment
- RILUZOLE
- Symptoms:
Spasticity - Baclofen, Tizanidine
Cramping & fasciculation - Quinine sulphate
Salivation & drooling - Amitriptyline,Scopolamine, irradiation
Pseudo bulbar affect - Amitriptyline - Resp dysfunction - NIV
- Swallow difficulty - thicken fluids, NPO, peg
long term survival in MND
Younger
male
limb symptoms (better than bulbar)
resp symp in MND that may be missed
Breathnessness Early morning headaches Daytime sleepiness, nocturnal agitation Nightmares Confusion
Hypoxic signs
Chorhea 2 types
Athetosis - slower, writhing movements
Ballism - proximal and large amplitude
Dystonia
Involuntary, sustained muscle contractions that result in twisting and repetitive movements or abnormal posture. [2]
tic
Brief, repeated, stereotyped movements which patients can suppress for a period of tim
Myoclonus
Brief, shock-like, involuntary movements caused by muscular contractions or inhibitions
Tardive Dyskinesia
Orobuccolingual, truncal or choreiform movements (grimacing/chewing)
Chronic exposure to antipsychotics/antiemetics (dopamine receptor blockers)
4 hypokinesia disorders
Parkinsons
Progressive nuclear palsy
Portico-Basal degneration
Multiple system atrophy
wha trinucelar repeat in fridrich’s ataxia
GAA
hereditary spinocerbral ataxia
progressive cerebellar syndrome
oculomotor retinal and pyramidal EP sensory cognitive and behavioural sam
what trinucelar repeat for huntigton
CAG
multiple sclerosis
immune-mediated inflammatory disease of the central nervous system, characterised by demyelination
proven risk factors
Female gender age 25-35 other A.I disease MHC 1 and 2 alleles HLA DRB1 MZT concordance: 20-40%
what is a relapse in MS called
Episode of neurological dysfunction lasting >24 hours in the absence of fever
Often lasts weeks to months
May gradually improve (remission)
May have residual disability following relapse
disseminated in space
Dissemination in space requires ≥1 T2 bright lesions in 2 or more locations: - Periventricular - infratentorial - juxtacortical - spinal cord
Dissemination in time
Dissemination in time can be established in one of two ways:
- a new T2 bright lesion and/or gadolinium-enhancing lesion when compared to a previous scan (irrespective of timing)
- presence of asymptomatic enhancing lesion and a non-enhancing T2 bright lesion on any one scan
B-interferon S/e
site necrosis, flu-like symptoms, abnormal LFTs (ALT), leukopaenia, anaemia
Gatiramer-acetate
injection site-reaction, post-injection chest pain, flushing, dyspnoea, palpitations, and/or anxiety
Natalizumab moa s/e
evelopment of progressive multifocal leukoencephalopathy
T cell lymphocyte inhibitor
Alemtuzumab S/e and moa
depletion of CD52
-expressing T cells, B cells, natural killer cells, and monocytes
S/e autoimmune disorders, including immune thrombocytopenia
Mitoxantrone s/e and use
Side-effects: cardiotoxicity, immunosuppression, possible link with colorectal Ca
USE Reserved for patients with rapidly advancing disease who have failed other therapies
Dimethyl Fumarate (oral)
neuroprotective and immunomodulatory properties
flushing and gastrointestinal symptoms, lymphopaenia, PML
Teriflunomide (oral)
disrupts the interaction of T cells with antigen presenting cells
diarrhoea, nausea, hair thinning, hepatotoxicity, teratogenicity
Fingolimod (oral)
alters lymphocyte migration, sequestration of lymphocytes in lymph nodes
small increased risk of infection, atrioventricular block, and possibly basal cell carcinoma.
spasticity in MS treatment
Baclofen (may also be given via intra-thecal pump)
Tizanidine :
Gabapentin
Clonazepam/diazepam: For cerebral-mediated spasticity
Botulinum toxin
Surgery: chronic epidural stimulation
Fatigue in MS
Amantidine
4 Aminopyridine
Antidepressnants
Modafinil
Bladder sphincter dysfunction
Anticholinergics/antimuscarinics
Botulinum toxin
Self intermittent catherisation
Suprapubic catheterisation
Bowel sphincter dysfunction
Laxatives Pro-kinetics Bowel stimulants Bulking agents Manual evacuation
Poor prognosis of MS
Early onset High lesion load Short interval between relapse Primary progressive MS Bowel/bladder symptoms at onset
Muscular disease definition
Neuromuscular disorders in which the primary symptom is muscle weakness due to dysfunction of muscle fiber
People with muscular disorders describe weakness doing specific movements (distinct from patients who complain of generalised weakness)
Ddx muscle weakness
CNS damage- Stroke, SOL Spinal cord injury or disease Anterior horn cell disease- MND, polio Peripheral nerve disease Neuromuscular junction disease- myasthenia gravis, Eaton Lambert syndrome
Myotonic dystrophy definition
Inherited (autosomal dominant) disease characterized by adult onset muscular dystrophy.
DM1: Trinucleotide repeat on chrom 19
DM2: tetranucleotide repeat - chromosome 3
Definition of myotonia
Slow relaxation of muscle following contraction (myotonia diminishes as disease progresses)
how to make diagnosis of muscle dystrophy
Genetic testing
CTG repeat in DM1
CCTG repeat in DM2
EMG repetitive myotonia (sounds like “dive-bomber”) Predominant in distal muscles
Muscle biopsy
Atrophy
Necrosis
Increased nuclei
signs of myotonic dystrophy
Finger grip myotonia- delay in letting go when shaking hand, or delay in loosening grip when asked to grips fingers
Percusssion myotonia- tapping over thenar eminence causes
Distal muscle weakness
Impaired extra-ocular muscle usage
Gynaecomastia
CF of cardiomyopathy- displaxed apex, murmurs, crepitations, etc.
Testicular atrophy
Ddx : TIA
Migraine Partial Seizure Syncope Vestibular Disorders Neuropathy and Radiculopathy Ocular Disorders Hypoglycaemia CNS Tumours
ABCD2 score
Age > 60
Blood Pressure > 140/80
Clinical (2 points for hemiparesis , 1 point for speech problem w/o weakness)
Duration 2 points > 60 minutes, 1 point 10-60 minutes
Diabetes
Interpretation of ABCD2 score
Score 6 to 7: High two-day stroke risk (8 percent)
Score 4 to 5: Moderate two-day stroke risk (4 percent)
Score 0 to 3: Low two-day stroke risk (1 percent)
Agnosia
inability to interpret sensation
MCA stroke presentation
Contralateral paralysis (Face and limbs) Contralateral sensory loss (Face and limbs) Aphasia/Dysphasia Homonymous hemianopia Agnosia Sensory neglect Apraxia (dressing/constructional)
Apraxia
Apraxia (dressing/constructional
Agnosia
inability to interpret sensation
Abulia
inability to act decisively
Posterior cerebral artery stroke
CENTRAL Mild hemiparesis Choreathetosis Intention tremor Thalamic syndrome- simultaneous sensory loss and anaesthesiae/parasthesiae
PHERIPHERAL Homonymous hemianopia/quadrantanopia Visual neglect Visual apraxia Prosopagnosia Visual hallucinations Memory abnormalities
BP should only be treated acutely in stroke if:
BP should only be treated acutely if: Patient is candidate for thrombolysis Severe HTN (SBP>220mmHg, DBP > 120mmHg) Co-existing ACS, AKI, acute CCF, acute aortic dissection Haemorrhagic stroke
Otherwise a higher BP - tolerated in ischemic stroke its permissive HTN
Lateral Medullary Syndrome
Ipsilateral Facial pain Impaired facial/limb sensation Nystagmus Ataxia Vertigo Diplopia Oscillopsia Impaired gag reflex Dysphagia Horner’s syndrome
Contralateral -Impaired pain and temperature sensation
Posterior cerebral artery stroke
CENTRAL Mild hemiparesis Choreathetosis Intention tremor Thalamic syndrome- simultaneous sensory loss and anaesthesiae/parasthesiae
PHERIPHERAL Homonymous hemianopia/quadrantanopia Visual neglect Visual apraxia Prosopagnosia Visual hallucinations Memory abnormalities
BP should only be treated acutely in stroke if:
BP should only be treated acutely if: Patient is candidate for thrombolysis Severe HTN (SBP>220mmHg, DBP > 120mmHg) Co-existing ACS, AKI, acute CCF, acute aortic dissection Haemorrhagic stroke
Otherwise a higher BP - tolerated in ischemic stroke its permissive HTN
blood pressure is >185/110 mmHg, treat with:
Labetalol IV, up to twice OR
Nicardipine drip
Malignant MCA syndrome
2-5 days post stroke Mortality 50-80% Clinical Predictors: Young age History of hypertension, heart failure, Raised WCC, Coma on admission Nausea, vomiting SBP> 180mmHg within first 24hrs
criteria for hemicrainectomy
- Age< 60
- NIHSS>15
- Decrease LOC >/=1 on item 1a of the NIHSS
< 45 hrs from onset(surgery should be undertaken < 48hrs from onset) - space occupying cerebellar infarcts
- At least 50% MCA territory involved on CT, with / without additional infarction in the territory of the anterior or posterior cerebral artery on the same side, or 145cm3 on DWI MRI
what location of stroke is worse
ACA and PCA
Best = lacunar
prognosis post stroke
Severity of stroke (NIHSS scale)
Site of stroke
co-morbidities,
Baseline function
Presence of continued risk factors (smoking, poor DM control, AF, etc.)
BMI - low or normal BMI confer poor prognosis
treatment of heamorragic stroke
Reversal of anticoagulant
- ABC, Tx infection, Early SALT review, BP monitor, seizure prophylactic,
Possible craniotomy
what is better for stroke CT OR MRI
Non-contrast CT brain ±CT angiogram (intracranial ± carotids/vertebrals) MRI brain (more sensitive for early infarct with FLAIR, less widely available)
