1
Q
What is epilepsy
A
Spontaneous, intermittent, abnormal electrical activity in the brain manifested as seizures.
2
Q
Types of partial seizures
A
- Simple partial (Focal seizure, fully aware)
- Complex partial (Focal seizure, impaired awareness)
- Partial seizure with secondary generalisation
3
Q
Types of generalised seizures
A
WHOLE BRAIN
- Absence
- Tonic-clonic (stiffness then movement)
- Myoclonic (sudden jerking)
- Atonic (loss of muscle tone, no LOC)
4
Q
Causes of seizures; Four broad categories
A
- Idiopathic
- Structural (scarring post TBI, space occupying lesion, stroke)
- Systemic (sarcoidosis, SLE, PAN)
- Non-epiletic (Trauma, bleed, raised ICP, EtOH/benzo withdrawal, metabolic disorder + fever, liver disease, infections, drugs, pseudoseizures)
5
Q
Epilepsy presentation
A
- Details of seizure (determine classification, length, tongue biting, incontinence)
- Prodome symptoms
- Triggers
- First episode/frequency of episodes
- Drugs/EtOH/sleep
6
Q
Epilepsy/seizure exam key points
A
- Neuro exam
- Evidence of focal brain lesion
- Non-neuro causes
- TBI
- Tongue
7
Q
Epilespy diagnosis and differentials
A
Dx - clinical +/- positive EEG
DDx
- Syncope (Orthostatic, Vasovagal, arrhythmia, cardiac)
- Hypoglycaemia
8
Q
Seizure investigations
A
- FBC, glucose, extended electrolytes, Cr, LFTs
- Urine tox
- CXR
- CT head if indicated
- EEG/MRI
- other Ix to rule out DDx
9
Q
Epilepsy non-pharmacological mangement
A
- Avoid triggers
- reduced EtOH/stop smoking and drugs
- Driving standdown (1yr no seizure-like activity)
- Education
- Referrals
10
Q
Epilepsy pharmacological mangement
A
Gereralised
- Sodium valporate (first line)
- Lamotrigine (second line)
(Levetriacetam, carbamazepine)
Partial +/- secondary generalised
- Carbamazepine
Pregnant or breastfeeding
- Lamotrigine
11
Q
What is motor neuron disease
A
Group of several disorders where motor neurons progressively degenerate
UMN and LMN are affected
***Eyes are not affected (differentiation from myasthenia gravis)
12
Q
motor neuron disease epidemiology
A
- Very rare
- M>F
- Mean age of onset = 60
- Prognosis 2-4years
13
Q
Types of motor neuron disease
A
- Amyotrophic Lateral sclerosis (UMN and LMN in 3 regions)
- Progressive bulbar palsy (Only cranial nerves IX - XII, causes speech and swallowing issues, tongue fasciulations)
- Primary Lateral sclerosis (Predominantly UMN)
14
Q
Presenation of motor neuron disease
A
> 40y/o
Stumbling gait
Foot drop
Weakness
Aspiration pneumonia
Swallowing difficulties
Fronto-temporal dementia
15
Q
Examination for motor neuron disease
A
Neuro exam
- UMN and LMN signs
- Speech
- Swallow
- Gait
- Memory/cognition
16
Q
motor neuron disease investigations
A
Mostly a clinical diagnosis
MRI +/- LP to exclude other causes
17
Q
motor neuron disease management
A
Non-pharmacological
- MDT: Neurologist, palliative care, PT, OT, SLT, dieticians, SW
Pharmacological
- Antiglutamatergic drugs (Riluzole)
- Diazepam for spasticity
18
Q
Multiple Sclerosis Onset and Risk Factors
A
- 20-40y/o
- F>M
- HLD-DRB1 has genetic component
- FHx
19
Q
What is multiple sclerosis?
A
Discrete plaques of demyelination occur throught the CNS caused by T cell mediated immune response.
Relapsing remitting (Most common). (Incomplete healing of demyelination) -> leads to axonal loss and secondary progressive MS. 80% enter this stage, 50% after ten years.
20
Q
Multiple Sclerosis Presentation
A
- Attacks = neuro defect >1hr, with >30days between
- USUALLY 1x Sx, Unilateral;
- Weakness
- Paraethesia of limb(s)
- Optic neuritis (Unilateral, pain on EM, Dec VA)
-Ataxia/Dysarthria/tremour (Charcot’s triad) - ++ Many other less common
- Usually full recovery between attacks, then gradually these remissions are incomplete
21
Q
What are the precipitating factors for MS flare?
A
- Precipitating factors (Heat, infection, fever, excersise)
22
Q
Multiple Sclerosis Diagnosis
A
Clinical Dx
Mcdonald’s criteria
- 2 acute episodes separated in time and place
- 1 acute episode + MRI evidence in different region
23
Q
Multiple Sclerosis Investigations
A
- MRI
- Evoked reponse screening (hearing, vision, somatosensory)
- CSF (Oligioclonal IgG bands on electrophoresis -> Inflammation)
24
Q
Multiple Sclerosis Management
A
Non-pharmacological:
- MDT
- Support groups
- Bed rest
Pharmacological:
- Steroids (for relapse, shortens, not disease altering)
- Interferons and monoclonal antibodies (decrease relapse frequency)
- Methotrexate (Can be tried)
- Sx relief
25
What are some medications that can be used in the symptom releif of MS?
Severe spasticity; Baclofen
Bladder dysf: Oxybutynin + amytryptline
Facial spasm: Carbimazepine
Tremor: Clonazepam or propranolol
26
What are the differential diagnoses when you have an apparent multiple CNS lesions?
- Sarcoidosis
- Small vessel ischaemia, multiple emboli,
stroke
- Spinal cord compression (various causes)
- Various other very complex diseases
- Spinal tumours
27
What is myasthenias gravis?
- Autoantibodies to nicotinic acetylcholine receptors on the post synaptic membrane of neuromuscular junctions.
= Stops muscle contraction
- Fatiguing muscle weakness in the following order: Extra-ocular > bulbar > face > neck > limb girdles > trunk
- Exacerbations and incomplete remissions are common.
- F (3rd decade of life) > M (7th decade of life).
- LMN
28
What are the examination findings for suspected for myasthenias gravis?
Observe:
- Ptosis
- Peek sign
- Snarling smile
Muscle fatigue
- Sustained upward gaze
- Counting aloud
- Hold arms above head
Reflexes intact, no sensory loss
Diplopia
Thymectomy scar
29
What PMHx is myasthenias gravis associated with?
o Difficult anaesthesia (Prolonged muscle weakness)
o Pneumonia
o Thymectomy
o Otherauto-immunediseases–SLE,
rheumatoid arthritis
30
What are the investigations you can perform for myasthenia gravis?
- **Antibodies**: Anti-AChR (90%)
- **Neurophysiology** : EMG - Decremental muscle response.
- **Thymoma investigations**: CXR, CT or MRI
- Spirometry for resp func.
- Associated conditions; LFTs, TFTs, ANA
31
Whats the sympatomatic management of myasthenias gravis?
- Anticholinesterase
o E.g.Pyridostigmine60-120mgPO up to 6x daily
o SE:increased salivation,lacrimation, vomiting, diarrhea
- Avoid drugs that impair NM transmission like gentamicin, procainamide
- Sudden worsening of respiratory symptoms
can be life threatening and treated with mechanical ventilation and plasmapheresis. Often precipitated by infection, so treat aggressively (not with aminoglycosides)
32
Whats the management of MG disease suppression?
Disease Suppression
- Relapses treated with prednisolone. (Given long term once anti-Ach inadequate) - Give osteoporosis prophylaxis.
Failed steroid treatment -> immunosuppression
o Azathioprine
o Methotrexate
o Rituximab in desperate cases
Thymectomy (because MG associated with
thymomas)
o If symptoms < 50 yrs, and ACH- antibody positive.
33
What are the differential diagnoses for proximal muscle weakness?
- Lambert-Eaton syndrome. Pre-synaptic
failure of release of acetylcholine caused by Small CC of lung. Muscle weakness improves on use.
- Polymyositis
- Acquired myopathy (hyperthyroid, SLE,
Cushing’s)
34
What is the definition of parkinsons disease?
A progressive and incurable movement disorder (neuro disease) characterized by Akinesia/ bradykinesia and one of Tremor, Rigidity, and Postural instability caused by degeneration of dopaminergic neurons of the pars compacta in the substantia nigra, causing decreased dopamine levels in the striatum (caudate nucleus and putamen).
35
What are the pro-dromal pre motor symptoms of parkinsons?
RAD x2
- Anosmia
- Depression/anxiety
- REM behavioral sleep disorder
- Autonomic affects (hypotension causing
postural instability, urinary incontinence, constipation)
- Dementia, visual hallucinations
- Restless legs
- Dribbling
36
Whats the motor presentation of parkinsons?
- Usually asymmetrical onset
- Slowness, stiffness, tremor
- Freezing, dyskinesias, wearing off
37
What is the aim of the exam for a patient with suspected parkinsons?
To differentiate parkinsons from Parkinsons +
38
What are the exam findings for a patient with parkinsons?
- Masked face
- Flexed posture (cant lie head down)
(Core features: TRAP)
- Tremor (Pill rolling, increase with distraction i.e movement of other hand and decrease with holding hand out)
- Rigidity (Cogwheel)
- Akinesia (bradykinesia, shuffle gate)
- Postural instability (Shuffle gate)
39
What are the extra tests for PD?
Glabellar tap
- Failure of attenuation of blink response
Weakness of upward gaze, loss of downward gaze = PSP
Micrographia
40
What are the ddx for PD?
1) Parkinsons plus syndrome
2) Drug induced
3) Toxin induced; Wilsons
41
What is PSP?
Progressive supranuclear palsy
Early postural instability, vertical gaze palsy, rigidity trunk > limbs, pseudo- bulbar palsy, symmetrical onset, tremor unusual.
42
What are the parkinsons plus syndrome?
- Propgressive supranuclear palsy (PSP)
- Lewy body dementia (Fluctuation cognition and hallucinations)
- Vascular parkinsons
- Multisystem atrophy (Autonomic features, rigid>tremour)
- Corticobasal degeneration (Rigid one limb)
43
What drugs can induced parkinsonism?
- Antipsychotics- haloperidol and lithium
- Dopamine receptor antagonists
o Prochlorperazine and
Metoclopramide
44
What are the investigations for suspected PD?
- CT or MRI if no tremor to exclude brain lesion
- Younger patients should have slit lamp for KF rings (Wilson’s) or serum copper
- Olfactory testing (also reduced in MSA)
- Review by neurologist if young or unusual
presentation
45
What is involved in the non-pharmacological tx of PD?.
- Education
- Exercise - PT- strength/speed/ROM/reduce falls, OT
- Multidisciplinary approach. Neurologist, PD
nurse, SW, GP, respite care,
- SLT-
dysphagia/voice volume, psych
46
What is involved in the pharmacological tx of PD?
- Treatment of non-motor symptoms
o Depression->SSRI’s
o Psychosis->quetiapine or olanzapine
- Sinemet
o Levodopa+ dopadecarboxylase (dopamine metabolizer) inhibitor.
- Dopamine agonists
o Ropinirole. Used as monotherapy to delay starting L-dopa in early stages.
o Apomorphine as a continuous infusion or as a rescue pen for freezing
- Anticholinergics
o Help with tremor.
47
What is the SE of using anticholinergics to manage tremor in PD patients?
SE: confusion, dry
mouth, dizziness, urinary retention.
48
What are the initial effects and SE of sinemet?
Initial response dramatic, efficacy reduces with time.
SE: dyskinesia, painful dystonias, nausea, psychosis.
49
What are the invasive options for tx of parkinsons?
- Deep brain stimulation – for younger
patients
- Surgical ablation of overactive basal ganglia
50
What are the stages and prognosis of PD?
Prodromal (non-motor sx) -> ?10-20 years
Preclinical (Anosmia, REM sleep disorder) ~2 years
Diagnostic (Parkinsonism with minimal fluctuation) (1-2 years)
Maintenance (L-dopa responsive, no postural instability) 5-10 years
Complex (Complex meds, fluctuation of dyskinesias, autonomic /psych manifestations) ~5 years
Palliative (Poor response to meds, reduced to L dopa monotherapy) ~ 2 years
51
Whats the definition of TIA?
Transient neurological deficit lasting < 24 hours, but usually resolve within 1 hour, caused by temporary occlusion of the cerebral circulation.
Suggest that a stroke is likely in the future, so management is very important
52
What are the causes of TIA?
- Atherothromboembolism o Most common
- Cardioembolism
o Mural thrombus postMI, AF, valve disease, prosthetic valves
- Hyperviscosity
o Polycythemia, elevated WCC, myeloma
53
What are the relevant findings in a TIA hx + exam?
- As per stroke territories
- Global events such as syncope and dizziness
are NOT typical of TIA
- Amaurosis fugax (progressive loss of vision
in one eye “like a curtain descending”
- Listen for carotid bruit, measure BP, listen
for murmurs, AF
54
What are the ddx for TIAs?
- Hypoglycaemia
- Migraine aura
- Focal epileptic seizure
- Syncope and hypotension
- Hyperventilation
- Vertigo +/- secondary nausea and ataxia
- MS
- Somatization
55
What investigations might you do for suspected TIA?
Bloods
- FBC, ESR, U+E’s glucose, lipids
Imaging
- CXR
- Carotid USS +/- angiography
- CT or diffusion weighted MRI
- Echo – foramen ovale or other holes?
ECG
56
What is the TIA stroke risk score criteria?
ABCD2
A- Age >60 (1)
B- BP > 140/90 (1)
C- Clinical features
-> Unilateral weak (2)
-> Speech disturb (1)
D- Duration
-> >1hr (2), <1hr (1)
D- Diabetes (1)
57
What is the non-pharmacological management of TIA?
Non-Pharmacological
- Diet, exercise
- Smoking cessation
- Avoid driving for 1/12
58
What is the pharmacological management for a TIA?
- Control CV risk factors
o Cautiously lower BP– target 140/85mmhg
o Statins
o ControlDM
o Smokingcessation
- Antiplatelet
o Aspirin 300mg daily or Clopidogrel 75mg daily
- Anticoagulation
o If cardiac emboli (e.g.from AF or
mitral stenosis)
59
What are the invasive potential treatments for things that cause TIA?
- Consider carotid endarterectomy if > 70%
stenosed and operative risk is good. Operating on 50 – 70% stenosis has some value if operative risk very low.
- Should be performed within 2 weeks of first presentation.
- Do not use antiplatelets beforehand.
- Carotid stenting is a good alternative if not
good for surgery
60
What is a stroke?
Stroke = Acute neurological deficit lasting > 24
hours
61
What are the causes of ischaemic stroke?
Ischaemic 85%
- Large artery atherosclerosis +
thromboemboli
- Cardioembolic
- Lacunar (thrombus in situ)
- More likely if carotid bruit, AF, past TIA, IHD
62
What are the causes of hemorrhagic stroke?
- Hypertension
- Berry aneurysm
- Coagulopathy e.g. APLS
- AV malformation
- More likely if meningism, severe headache
and coma within hours.
Subarachnoid 5%- sudden severe headache
Other = Watershed infarct (after sudden drop in BP)
63
What are the signs and symptoms of an anterior circulation stroke?
- Internal Carotid Artery
o Hemiparesis and hemianaesthesia on opposite side of body
o Homonymous hemianopia
o Dysphasia
- Anterior Cerebral Artery
o Hemiparesis L > A
o Sensory loss leg only
o Change in personality, mood, behavior
and social inhibition.
- Middle Cerebral Artery
o Left MCA – R sided weakness involving lower part of face, arm > leg with dysphasia
o RightMCA–Lsided weakness involving lower part of face, arm > leg with visual and/or sensory neglect
64
What are the signs and symptoms of a posterior circulation stroke?
- Posterior Cerebral Artery
o Homonymous hemianopia
o Parietal deficits–spatial skills, recognition
o Temporal deficits–memory, mood, aggression
- Vertebrobasilar arterial System
o Midbrain
3rd and 4th CN deficits same side Weakness and sensory loss opp side
o Pons
5th and 6th CN deficits same side Weakness and sensory loss opp side
o Medulla
9th, 10th, 11th CN deficits same side Weakness and sensory loss opp side
o Cerebellum 'DASHING'
Dysdiadochokinesia and dysmetria, ataxia, slurred speech, hypotonia, intention tremor, nystagmus, gait abnormality
65
What are the ddx for a possible stroke?
- Migraines with focal seizures
- Seizure with post-ictal paresis (Todd’s
paresis)
- Haemorrhage into mass
- Multiple Sclerosis
- Compressive mononeuropathy
- Brain tumours
- Drug overdose
- Hepatic encephalopathy
- Abscesses
- Toxoplasmosis
- Head injury
- Hypoglycaemia
66
What are the investigations for a possible stroke?
- CT, MRI
- Bloods: FBC, U+E, Lipids, Coags
- ECG (AF)
Other:
- Carotid USS (non disabled)
- Thrombophilia screen (<50)
- ECHO (Cardioembolic consideration)
67
Whats the primary prevention for stroke?
Control risk factors
- HTN, DM, lipids
- Exercise, diet, quit smoking
68
Whats the management of an acute ischaemic stroke?
- <1hr = protect airway, control BP
carefully (autoregulation impaired so a decrease in BP can cause hypoperfusion)
- Checl blood glucose,
- urgent CT,
- antiplatelets if excluded hemorrhagic,
Thrombolysis
- Thrombectomy if suitable candidate – (prior function, <6hrs onset for AC, <24hrs for PC)
- Thrombolysis with IV Alteplase
o If <4.5hrs
o If previous independent
o Exclusion –bleed on CT, BP>185/110, recent stroke or MI, surgery or trauma within 30 days
o 10% bolus, 90% over one hour
o Monitor BP, neuro obs and temp
- Clopidogrel (After 24 hours if
thrombolysed) + aspirin if extensive stroke for 3weeks (only after ruled out haemorrhagic)
- Consider heparin
- DVT prophylaxis
- NBM until swallow assessment +/-
parenteral fluids
- Driving restriction
- Cerebellar infarcts can swell – monitor
closely
69
Whats the treatment of acute heamorrhagic stroke?
- Stop antithrombotic
- Reverse anticoagulation
- Neurosurgical referral
70
Whats the secondary prevention for stroke?
- Clopidogrel 75mg (better than aspirin)
- Control HTN – continue regular meds, delay new meds until 72 hours.
- Statins 40mg regardless of lipids
- Smoking cessation
- Consider carotid endarterectomy if >70%
stenosed
- If in AF, consider anticoagulation after 2
weeks.
71
What is the definition of a polyneuropathy?
Disorders of peripheral or cranial nerves; usually symmetrical & widespread, often with distal weakness and ‘glove & stocking’ sensory loss.
72
How are polyneuropathies classified?
Classified by course (acute/chronic), by function (sensory/motor/autonomic/mixed), or by pathology (demyelinating/axonal degeneration/both).
i.e. GB acute demyelinating motor
73
What are the main causes of motor polyneuropathy and sensory polyneuropathy?
Mostly Motor: GBS, Lead poisoning, Charcot-Marie- Tooth
Mostly Sensory: DM, renal failure, leprosy
74
What are the causes of polyneuropathies?
Metabolic:
- DM
- Renal failure
Nutritional;
- Vitamin B1, B12 deficiency (Ethanol abuse)
Inflam:
GBS
Many more...
75
What are you asking for in a suspected sensory polyneuropathy hx?
SENSORY NEUROPATHY: - Numbness, tingling
- Burning pain (alc, DM) - Glove & stocking
- Check functional ability
- Signs: Tm, joint deformity
76
What are the signs of a suspected motor polyneuropathy?
MOTOR NEUROPATHY:
- Often progressive
- Weak clumsy hands
- Difficulty walking (falls)
- Difficulty breathing (reduced VC)
- Signs: LMN signs- wasting, weakness distally (foot/hand drop), reduced/absent reflexes
77
What about cranial nerve or autonomic impact in the hx of a polyneuropathy?
CRANIAL NERVES:
- swallowing or speaking difficulty
AUTONOMIC NEUROPATHY: (SNS & PSNS)
- Postural hypotension (S)
- Erectile dysfunction (P)/Ejaculatory failure (S)
- Decreased sweating (S)
- Constipation, nocturnal diarrhea, urine retention (P)
- Horners (S)
- Homes Adie pupil (P)
78
What investigations do you perform for a suspected polyneuropathy?
Bloods:
- FBC, ESR, glc, U&E, TSH, B12/folate, ANA,
ANCA
CXR
Urine analysis
Consider LP +/- specific studies
Nerve conduction studies: demyelinating vs axonal
79
What are the principles of managing a polyneuropathy?
- Treat cause
- PT,OT
- Foot care & show choice education
- Joint splinting to prevent contractures
- GBS/CIDP IV Ig; Vasculitis steroids
- Neuropathic pain: amitriptyline, gabapentin
80
What is the definition of GBS?
Most common “acute inflammatory demyelinating polyneuropathy” characterised by; motor difficulty, absence of reflexes, paraesthesias without sensory loss.
Symptoms progress for 4 weeks then slow recovery
81
What are the causes of GBS?
Usually caused by auto-Abs triggered by antecedent infection (C. jejuni, CMV, EBV, M. pneumonia).
82
How does GBS present?
- Progressive muscle weakness (lower-> upper; proximal->distal), acutely over days
- Flaccid paralysis
- Areflexia
- Paraesthesia in feet/hands (mild, before
weakness)
- Pain: legs, back
- Resp: SOB-OE, resp muscle weakness
Think cranial nerve impacted:
- Speech: facial & oropharyngeal weakness –
slurring
- Face: facial droop, dysphagia
- Eyes: diplopia, extra-occular weakness,
ptosis
Think ANS:
- Autonomic dysfunction (sweating,
tachycardia, BP changes, arrhythmias)
83
What investigations might you perform for suspected GBS?
Nerve conduction studies:
- Slowing of velocities
LP:
- Raised CSF protein (>5.5g/L)
Bloods:
- Raised AST & ALT, slight bili rise
- Anti-ganglioside Ab; helps differentiate
subtype (unknown in AIDP)
- Serology Campylobactor, CMV, EBV, Mycoplasma
- Spirometry:
- 6hr intervals at bedside
- may show decreased Vc, maximal inspiratory P or expiratory P.
Imaging:
- MRI to rule out spinal cord pathology
84
What is the criteria for GBS?
1. Progressive muscle weakness in limbs
2. Areflexia (hypo-)
3. +/- Progressive over 2-4wks, symmetry,
mild sensory change, CN involved. Recovery begins 2-4wks after plateau. Autonomic changes, no fevers, CSF/EMG findings.
85
What is the treatment for GBS?
- IV Ig 0.4g/kg/24hrs for 5 days
o CI:IgA def,renal failure
- Supportive:
Plasma exchange
- Ventilate (bulbar/bilateral CNVII palsy, dysautonomia) if resp involvement
- DVT prophylaxis
- Monitor vitals
- Analgesia: neuropathic type
- Physio input
86
Whats the prognosis of GBS?
85% good recovery. 20% mortality if ventilated. Poorer outcomes if older age, severe Sx, rapid onset, atrophy, need for ventilation, high antibody titre
87
What are the potential complications of GBS?
Fatigue
Resp Failure (30%)
Bladder areflexia
Adynamic ileus
Paralysis 15% - strengthening exercises in acute rehab
DVT risk – 2 to immobilization
88
What is a variant of GBS?
*Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) = variant of GBS, characterized by a sower onset & recovery.
89
What features of a presentation favor a myopathy?
- Gradual onset
- Symmetrical proximal weakness (difficulty combing hair, climbing stairs)
- Preserved tendon reflexes
- Pain at rest, local tenderness (inflam myopathy) - Oddly firm muscles (DMD)
- Lumps - tendon rupture, muscle herniation
90
What investigations might you do for a myopathy?
- Bloods: ESR, CK, AST, LDH, TSH - EMG
- DNA analysis (muscle Bx)
91
What are muscular dystrophies? and three examples;
Group of diseases with progressive degeneration of specific muscle groups.
1) Duchennes muscular dystrophy
2) Beckers muscular dystrophy
3) Facioscapulohumeral Muscular Dystrophy
92
Describe duchennes muscular dystrophy:
- Sex linked male only
- Dysfunctional dystrophin protein.
- Presents ~4years
- Death by 20
- Clumsy walking, difficulty standing, resp failure,
- Psuedohypertrophy in calves.
93
What are a couple facts about facioscapulohumeral muscular dystrophy?
- Weak face, cant puff cheeks
- scapular winging
- Scoliosis
- Difficulty raising arms above head
- Horizontal clavicles
94
What is beckers muscular dystrophy?
Similar to DMD but milder and better prognosis
95
What are myotonic disorders?
Causes muscle spasm (myotonia). Long chains of central nuclei in muscle fibers on histology.
-> Dystrophia Myotonica
96
What are inflammatory myopathies?
-Inclusion body myositis most common
-Muscle weakness (quads, finger flexors or pharyngeal muscles first)
-Biopsy shows inclusion bodies
-Polymyositis and dermatomyositis are also inflammatory myopathies but are included under the ‘Rheumatology’ section
97
What are the doses for the common epilespy meds?
- Sodium valproate 300mg BD (10mg/kg IV)
- Levetiracetam 250mg daily (same IV)
- Carbamazepine 100mg BD
98
What are the doses of the common antiplatelet drugs?
- Aspirin 300mg daily
- Clopidogrel 75mg daily
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