Neurology Flashcards
Parkinsonism Examination
(inspection/arms/eyes/extras/completion)
Gait: slow initiation, shuffling, festination, absent arm swing, stooped posture, hurried steps, retropulstion
Inspection: Hypominia (vFacial expression)
- Extrapyramidal posture
- Asymmetrical resting tremor: 5Hz (exacerbated by counting backwards)
- Ask pt to hold hands out in front of them, Fingers spread (Parkinsonian T-improves, BET-worsens)
Arms:
- Bradykinesia (touch thumb to each finger in turn as quickly as possible)
- Tone:
- cogwheel rigidity (‘shake’ hand)
- lead pipe rigidity (flex and extend elbow, whilst tapping knee with other hand (synkinesis))
- Power: n
- Reflexes: n
- Co-ordination: n (abnormal in MSA)
Eyes: Movement: nystagmus (MSA) + Vertical gaze palsy (progressive supranuclear palsy) + Saccades
Extra:
- Glabellar tap- Ask pt to fx eyes on a point on the wall “I am going to tap on your forehead” Tap repeatedly between their eyes with your index Finger Look for failure of attenuation of the blink response
- Speech: state name and date of birth, listen for slow monotonous speech,
- Write (name and address-micrographia), draw spiral
- Functional: do up a button/handle coins/motion of turning a tap BP (supine and erect)
Complete:
- Hx
- Full neuro examination
- MMSE
- Drug chart
- Abdo; Hepatomegaly + CLD
Parkinsonism Viva Causes
- Idiopathic PD
- Parkinson Plus Syndromes
- Progressive supranuclear palsy
- MSA
- Lewy Body Dementia
- Corticobasilar degeneration
- Multiple infarcts in the substantia nigra
- Wilson’s disease
- Drugs: neuroleptics and metoclopramide
Parkinsonism Viva Hx
- Symptoms: tremor, rigidity, akinesia
- Autonomic
- Postural hypotension
- Urinary problems, constipation
- Hypersalivation
- ADLs
- Handwriting, buttons, shoe-laces
- Getting in and out of a car
- Sleep
- Turning in bed
- Insomnia
- Daytime sleepiness
- Complications
- Depression
- Drug SEs: esp. motor fluctuations
- Cause
- Sudden onset
- Eye or balance problems
- Visual hallucinations, ↓ memory
- DH
- FH
Parkinsonism Viva Ix
Bloods
Caeruloplasmin: ↓ in Wilson’s
Imaging
CT / MRI: exclude vascular cause
DaTscan
- Ioflupane I123 injection
- Binds to dopaminergic neurones and allows visualisation of substantial nigra
- Can exclude other causes of tremor: e.g. BET
Parkinsonism Viva Mx
- General
- MDT: neurologist, PD nurse, physio, OT, social worker, GP and carers
- Assess disability e.g. UPDRS: Unified Parkinson’s Disease Rating Scale
- Physiotherapy: postural exercises
- Depression screening
- Specific
- L-DOPA + Carbidopa or benserazide
- Da agonists: ropinerole, pramipexole
- Apomorphine: SC rescue drug
- MOA-B inhibitors: rasagiline
- COMT inhibitors: tolcapone
- Amantidine
- Anti-muscarinics: procyclidine
- Adjuncts
- Domperidone: nausea
- Quetiapine: psychosis
- Citalopram: depression
- Other
- Deep brain stimulation
- Basal ganglia disruption
Parkinsonism Viva pathophysiology
Destruction of dopaminergic neurones in pars compacta of substantia nigra.
- β-amyloid plaques
- Neurofibrillary tangles: hyperphosphorlated tau
Parkinsonism Viva features
(TRAPPS PD)
Asymmetric onset: side of onset remains worst
- Tremor: ↑ by stress, ↓ by sleep
- Rigidity: lead-pipe, cog-wheel
- Akinesia: slow initiation, difficulty c¯ repetitive movement, micrographia, monotonous voice, mask-like face
- Postural instability: stooped gait c¯ festination
- Postural hypotension: + other autonomic dysfunction
- Sleep disorders: insomnia, EDS, OSA, RBD
- Psychosis: esp. visual hallucinations
- Depression / Dementia / Drug SEs
Parkinsonism Viva autonomic dysfuctions
Combined effects of drugs and neurodegeneration
- Postural hypotension
- Constipation
- Hypersalivation → dribbling (↓ ability to swallow saliva)
- Urgency, frequency, nocturia
- ED
- Hyperhidrosis
Parkinsonism Viva L-Dopa Drug SEs
(DOPAMINE)
- Dyskinesia
- On-Off phenomena = Motor fluctuations
- Psychosis
- ABP↓
- Mouth dryness
- Insomnia
- N/V
- EDS (excessive daytime sleepiness)
- *End-of-dose**: deterioration as dose wears off w progressively shorter benefit.
- *On-Off effect**: unpredictable fluctuations in motor performance unrelated to timing of dose.
Parkinsonism Viva PLUS syndromes
PSP: +postural instab + speech disturb (?psudobulbar palsy) + palsy vertical gaze
MSA: Autonomic + cerebellar and pyramidal + rigidity>tremor
LBD: fluctuating cognition + visual hallucinations
Corticobasilar degeneration: aphasia, dysarthria, apraxia + akinetic rigidity + asterognosis + alien limb
Parkinsonism Viva: Differential of Tremor
- Resting: parkinsonism
- Intention: cerebellar
- Postural = Worse c¯ arms outstretched
- BET
- Endocrine: ↑T4
- Alcohol withdrawal
- Toxins: β-agonists
- Sympathetic: anxiety
Benign Essential Tremor
- AD
- Occur with movement and worse c¯ anxiety, caffeine
- Doesn’t occur c¯ sleep
- Better c¯ EtOH
- Treat with beta blockers
Cerebellar syndrome examination
Gait, arms, DANISH, completion
-
Inspect:
- bruising/scars (recurrent falls)
- Symmetry, muscle wasting, fasciculations (LMN lesion)
-
daNiSh:
- Nystagmus (&rapid saccades)
- Slurred speech:
- baby hipopotamous-slurring
- Read something aloud- stacatto speech)
-
ULEx:
- Tone: Hypotonia
- Power: low power may pause pseudo co-ordination problems
- Coordination:
- Rebound (dysmetria), bound test. Ask pt to put arms out straight in front, palms down and close eyes“Keep your arms in that position”Push each arm down in turn ~10cm then release itWatch for arm bouncing back up to beyond original position
- Finger nose test: past pointing, dysmetria, intention tremor
- -Dysdiadokinesis: ataxia
-
?LL:
- (Tone hypotonia)
- (Power (?reduced))
- (Co-ordination:
- foot tapping (dysdiadokinesis)
- Heel-shin (intention tremor, dysmetria)
-
Posture:
- Truncal ataxia: Assess stability sitting: Sit on side of bed+Ask to cross arms in front and sit still. If stable: assess stability standing, feet together and arms by sides
- Romberg’s test (positive in patients with sensory ataxia, negative in cerebellar ataxia nb low specificity and in cerebellar disease often unsteady with eyes open)
- Gait: wide-based, unsteadiness with lateral veering, irregular steps, heel-toe (v.difficult if cerebellar lesion)
-
Completion:
- Full neuro exam
- CN; brainstem stroke/MS/CPA lesion
- Peripheral NS; MS
- Signs of CLD: wilsons
- Drug chart: phenytoin
- Full neuro exam
Cerebellar syndrome viva Causes
DAISIES
- Demyelination
- Alcohol
- Infarct: brainstem stroke
- SOL: e.g. schwannoma + other CPA tumours
- Inherited: Wilson’s, Friedrich’s, Ataxia Telangiectasia, VHL
- Epilepsy medications: phenytoin
- System atrophy, multiple
Cerebellar syndrome viva nystagmus: cerebellar Vs vestibular origin
- Cerebellar Cause
- Fast phase towards lesion
- Maximal looking towards lesion
- Vestibular Cause
- Fast phase away from lesion
- Maximal looking away from lesion
Cerebellar syndrome viva Hx
- MS: paraesthesia, visual problems, muscle weakness
- Alcohol consumption
- Infarct: onset, stroke risk factors
- Schwannoma: hearing loss, vertigo, tinnitus, ↑ICP
- FH
- DH
Cerebellar syndrome viva Ix
- ECG: Arrhythmia
-
Bloods
- EtOH: FBC, U+E, LFT
- Thrombophilia: clotting
- Wilson’s: ↓ caeruloplasmin
- CSF: Oligoclonal bands
- Imaging: MRI is best to visualise the posterior cranial fossa
- CPA lesion: pure tone audiometry
Cerebellar syndrome viva Mx
-
General
- MDT: GP, neurologist, radiologist, neurosurgeon, specialist nurses, physio, OT
- CV Risk
- ↓ EtOH
-
Specific
- MS: methylprednisolone
- EtOH: Pabrinex, tapering course of chlordiazepoxide
- Infarct: consider thrombolysis
- Schwannoma: gamma-knife, surgery
- Wilson’s: penicillamine
Cerebellar syndrome viva Lateral medullary syndrome (wallenberg’s)
DANVAH
Cerebellar syndrome viva Vestibular schwannoma
Pathophysiology
- Benign, slow-growing tumour of superior vestibular nerve
- SOL → CPA syndrome: 80% of CPA tumours
- Assoc. c¯ NF2
Presentation
- Unilat SNHL, tinnitus ± vertigo
- ↑ICP: headache
- Ipsilateral CN 5, 6, 7 and 8 palsies and cerebellar signs
- Facial anaesthesia + absent corneal reflex
- LR palsy
- LMN facial nerve palsy
- SNHL
- DANISH
Cerebellar syndrome viva CPA Tx Ddx
- Vestibular Schwannoma
- Meningioma
- Cerebellar astrocytoma
- Metastases
Cerebellar syndrome viva Von Hippel-Lindau Syndrome features
- Renal cysts
- Bilateral renal cell carcinoma
- Haemangioblastomas
- Often in cerebellum → cerebellar signs
- Phaeochromocytoma
- Islet cell tumours
Cerebellar syndrome viva Friedrich’s ataxia Pathophysiology and features
- Pathophysiology
- Auto recessive mitochondrial disorder
- Progressive degeneration of
- Dorsal column
- Spinocerebellar tracts and cerebellar cells
- Corticospinal tracts
- Onset in teenage years
- Assoc. c¯ HOCM and mild dementia
- Main Features
- Pes cavus
- Bilateral cerebellar ataxia
- Leg wasting + areflexia but extensor plantars
- Loss of vibration and proprioception
- Additional Features
- High-arched palate
- Optic atrophy and retinitis pigmentosa
- HOCM: ESM + 4th heart sound
- DM in 10%: dip the urine
Ataxia Telangiectasia Viva
- Autosomal recessive
- Defect in DNA repair
- Onset in childhood / early adult
Features
- Progressive ataxia
- Telangiectasia: conjunctivae, eyes, nose, skin creases
- Defective cell-mediated immunity and Ab production
- Infections
- Lymphoproliferative disease
Cerebellar syndrome viva wilsons features (CLANK)
- AR mutation of ATP7B gene on Chr13
Features: CLANK
- Cornea: Keiser-Fleischer rings
- Liver: CLD
- Arthritis
- Neuro: parkinsonism, ataxia, psychiatric problems
- Kidney: Fanconi’s syn
UMN signs Ex
Inspection/gait/UMN signs/completion
Inspection
- Walking aids
- May have disuse atrophy and contractures
- Limb position
- Leg: extended, internally rotated c¯ foot plantar flexed
- Arm: flexed, internally rotated, supinated
Gait
- Unilateral → circumducting
- Bilateral → scissoring
UMN Signs
- ↑ tone
- Pyramidal distribution of weakness
- Leg: extensors stronger than flexors
- Arm: flexors stronger than extensors
- Hyper-reflexion
- Extensor plantars
Sensation:
- Examine for sensory level: suggests cord lesion
Completion
- CN: evidence of MS
- Cerebellum: evidence of MS
UMN Viva Bilateral LL: spastic paresis
common/other/mixed UMN and LMN
Common
- MS
- Cord compression
- Cord Trauma
- CP
Other
- Familial spastic paraparesis
- Vascular: e.g. aortic dissection → Beck’s syndrome
- Infection: HTLV-1
- Tumour: ependymoma
- Syringomyelia
Mixed UMN and LMN Features
- MND
- Ataxia, Friedrich’s
- SCDC: B12
- Taboparesis
UMN Viva unilateral LL
hemisphere and hemicord
Hemisphere → Spastic Hemiparesis
- Stroke
- MS
- SOL
- CP
Hemicord → Spastic Hemiparesis or Monoparesis
- MS
- Cord Compression
UMN Viva Hx
- MS: tingling, eye problems, ataxia, other weakness
- Cord compression: back pain, fever, wt. loss
- Trauma
- FH
UMN Viva Ix; Imaging & Causes: MS, Compression, SCDC
MRI: Cord and brain
Further Ix Depend on Cause
- MS
- LP: oligoclonal bands
- Abs: MBP, NMO
- Evoked potentials
- Compression
- FBC: infection
- CXR: malignancy
- DRE
- SCDC
- B12 level
- Pernicious anaemia Abs: IF, parietal cell
UMN: Mx (supportive)
Supportive
- MDT: GP, neurologist, radiologist, neurosurgeon, specialist nurses, physio, OT
- Orthoses
- Mobility aids
- Urinary: ICSC
- Contractures: baclofen, botulinum injection, physio
Cord compression
Features, causes, Ix, Mx
Key Features
- Pain
- Local, deep
- Radicular
- Weakness
- LMN @ level
- UMN below level
- Sensory level
- Sphincter disturbance
Causes
- Trauma: vertebral #
- Infection: epidural abscess, TB
- Malignancy: breast, thyroid, bronchus, kidney, prostate
- Disc prolapse: above L1/2
Ix
- MRI is definitive modality
- CXR for primaries
Mx
- This is a neurosurgical emergency
- Malignancy
- Dexamethasone IV
- Consider chemo, radio and decompressive laminectomy
- Abscess: abx and surgical decompression
Cauda equina lesion
- pain/weakness/sensation/sphincters*
- Causes*
- Pain
- Back pain
- Radicular pain down legs
- Weakness
- Bilateral flaccid, areflexic lower limb weakness
- Sensation
- Saddle anaesthesia
- Sphincters
- Incontinence / retention of faeces / urine
- Poor anal tone
Causes:
- Trauma: vertebral #
- Infection: epidural abscess, TB
- Malignancy: breast, thyroid, bronchus, kidney, prostate
- Disc prolapse: below L1/2
Anterior spinal artery/Beck’s syndrome
what/causes/effect
- Infarction of spinal cord in distribution of anterior spinal artery: ventral 2/3 of cord.
- Causes: Aortic aneurysm dissection or repair
- Effects
- Para- / quadri-paresis
- Impaired pain and temperature sensation
- Preserved touch and proprioception
Human T-lymphotropic virus-1
- Retrovirus
- ↑ prevalence in Japan and Caribbean
Features
- Adult T cell leukaemia / lymphoma
- Tropical spastic paraplegia / HTLV myelopathy
- Slowly progressing spastic paraplegia
- Sensory loss and paraesthesia
- Bladder dysfunction
Syringomyelia
Characteristics, causes, cardinal signs, other signs
Characteristics
- Syrinx: tubular cavity in central canal of the cord.
- Symptoms may be static for yrs but then worsen fast
- e.g. on coughing, sneezing as ↑ pressure → extension
- Commonly located in cervical cord
- Syrinx expands ventrally affecting:
- Decussating spinothalamic neurones
- Anterior horn cells
- Corticospinal tracts
Causes
- Blocked CSF circulation c¯ ↓ flow from posterior fossa
- Arnold-Chiari malformation (cerebellum herniates through foramen magnum)
- Masses
- Spina bifida
- 2O to cord trauma, myelitis, cord tumours and AVMs
- *Cardinal Signs**
1. Dissociated Sensory Loss - Loss of pain and temperature → scars from burns
- Preserved touch, proprioception and vibration.
- Root distribution reflects syrinx location
- Usually upper limbs and chest: “cape”
- Wasting/weakness of hands ± Claw hand
- Loss of reflexes in upper limb
- Charcot joints: shoulder and elbow
* *Other Signs**
- UMN weakness in lower limbs c¯ extensor plantars
- Horner’s syndrome
- Syringobulbia: cerebellar and lower CN signs
- Kyphoscoliosis
- *Ix**: MRI spine
- *Surgery:** Decompression at the foramen magnum for Chiari mal
Acute stroke
definition and pathogenesis
Definition
- Rapid onset focal neurological deficit of vascular origin lasting >24hrs.
Pathogenesis
- Ischaemic: 80%
- Atheroma: large or small vessel
- Embolism: cardiac or atherothromboembolism
- Haemorrhagic: 20%
Stoke clinical features
Bamford classification (/Oxford Stroke Classification)
TACS: carotid / MCA and ACA territory
- Hemiparesis and/or hemisensory deficit
- Homonymous hemianopia
- Higher cortical dysfunction
- Dominant: aphasia
- Non-dominant: neglect, apraxia
PACS: carotid / MCA and ACA territory
- 2/3 of TACS criteria, usually
- Homonymous hemianopia
- Higher cortical dysfunction
POCS: vertebrobasilar territory
Any of:
- Cerebellar syndrome
- Brainstem syndrome
- Homonymous hemianopia
LACS: infarct around basal ganglia, internal capsule, thalamus and pons
- Pure motor: post. limb of internal capsule
- Pure sensory: post. thalamus (VPL)
- Mixed sensorimotor: internal capsule
- Dysarthria / clumsy hand
- Ataxic hemiparesis: ant. limb of internal capsule
Acute stroke Ddx
- Head injury
- ↑ or ↓ glucose
- SOL
- Infection
- Drugs: e.g. opiate OD
Acute stroke Mx
Resuscitate
- Ensure patent airway: consider NGT
- NBM until swallowing assessed by SALT
- Don’t overhydrate: risk of cerebral oedema
- BM: exclude hypoglycaemia
Monitor
- Glucose: 4-11mM: sliding scale if DM
- BP: Rx of HTN can → ↓ cerebral perfusion
- Neuro obs
Bloods
- FBC: infection (sepsis may → stroke)
- U+E: electrolyte disturbances may mimic stroke
- Glucose: exclude hypoglycaemia
- Clotting: ↑ or ↓ INR may indicate cause
Imaging
- Urgent CT/MRI
- Diffusion-weighted MRI is most sensitive for acute infarct
- CT will exclude primary haemorrhage
Medical
- Consider thrombolysis if 18-80yrs and <4.5hrs since onset of symptoms
- Alteplase (rh-tPA)
- → ↓ death and dependency (OR 0.64)
- CT 24h post-thrombolysis to look for haemorrhage
- Aspirin 300mg PO/PR once haemorrhagic stroke excluded ± PPI
- Clopidogrel if aspirin sensitive
Surgery
- Neurosurgical opinion if intracranial haemorrhage
- May coil bleeding aneurysms
- Decompressive hemicraniectomy for some forms of MCA infarction.
Stroke Unit
- Specialist nursing and physio
- Early mobilisation
- DVT prophylaxis
- *Secondary Prevention**
- *Rehabilitation**
Absolute CI to thrombolysis
Contraindications to thrombolysis
- active internal bleeding
- recent haemorrhage, trauma or surgery (including dental extraction)
- coagulation and bleeding disorders
- intracranial neoplasm
- stroke < 3 months
- aortic dissection
- recent head injury
- pregnancy
- severe hypertension
Side-effects
- haemorrhage
- hypotension - more common with streptokinase
- allergic reactions may occur with streptokinase
Non-acute stroke;
‘work up’/Ix
ECG ± 24hr Tape
- Arrhythmia
- Old ischaemia
Bloods
- FBC: ↑ or ↓ Hb
- U+E: association c¯ renovascular disease
- Glucose: exclude DM
- Lipids: CV risk
- Clotting and thrombophilia screen
- Vasculitis: ESR, ANA
Thrombophilia Screen
- FBC, clotting, fibrinogen concentration
- APC resistance / F5 Leiden
- Lupus anticoagulant
- Anti-cardiolipin Abs
- Assays for protein C and S and AT3 activity
- PCR for prothrombin gene mutation
Imaging
- CXR
- Cardiomegaly 2O to HTN
- Aspiration
- Carotid doppler
- Echo
- Mural thrombus
- Regional wall motion abnormality
- ASD, VSD: paradoxical emboli
Non-acute stroke
Secondary prevention
- Risk factor control e.g. Start a statin after 48h
- Aspirin / clopi 300mg for 2wks after stroke then either
- Clopidogrel 75mg OD (preferred option)
- Aspirin 75mg OD + dipyridamole MR 200mg BD
- Warfarin/DOAC instead of aspirin/clopidogrel if
- Cardioembolic stroke or chronic AF
- Start from 2wks post-stroke (INR 2-3)
- Don’t use aspirin and warfarin together.
- Carotid endarterectomy if good recovery + ipsilat stenosis ≥70%
Non-acute stroke
rehabilitation (MENDS)
Rehabilitation: Must occur on a dedicated stroke unit
MENDS
- MDT: physio, SALT, dietician, OT, specialist nurses, neurologist, family
- Eating
- Screen swallowing: refer to specialist
- NG/PEG if unable to take oral nutrition
- screen for malnutrition (MUST tool)
- Supplements if necessary
- Screen swallowing: refer to specialist
- Neurorehab: physio and speech therapy
- Botulinum can help spasticity
- DVT Prophylaxis
- Sores: must be avoided @ all costs
Non-acute stroke;
prognosis@1yr
- 10% recurrence
- PACS
- 20% mortality
- 1/3 of survivors independent
- 2/3 of survivors dependent
- TACS is much worse
- 60% mortality
- 5% independence
MS definition and dignosis
A chronic inflammatory condition of the CNS characterised by multiple plaques of demyelination disseminated in time and space
Diagnosis is CLINICAL: Demonstration of lesions disseminated in time and space May use McDonald Criteria
MS epidemiology
Lifetime risk: 1/1000
Age: mean @ onset = 30yrs
Sex: F>M = 3:1
Race: rarer in blacks
MS pathophysiology
CD4 cell-mediated destruction of oligodendrocytes → demyelination and eventual neuronal death. Initial viral inflamation primes humoral Ab responses vs. MBP. Plaques of demyelination are hallmark
(Aetiology: Genetic (HLA-DRB1), environmental, viral (EBV))
MS classifications
- Relapsing-remitting: 80%
- Secondary progressive
- Primary progressive: 10%
- Progressive relapsing
MS Examination Presentation (TEAM)
Tingliing Eye; optic neuritis (vCentral vision + eye movement pain)
Ataxia + other cerebellar signs
Motor; usually spastic parapesis
MS Features
(sensory, motor, eyes, cerebellum, GI, GU, Lhermiutte’s)
- Sensory:
- Dys/paraesthesia
- ↓ vibration sense
- Trigeminal neuralgia
- Motor:
- Spastic weakness
- Transverse myelitis
- Eye:
- Diplopia
- Visual phenomena
- Bilateral INO
- Optic neuritis → atrophy
- Cerebellum:
- Trunk and limb ataxia
- Scanning dysarthria
- Falls
- GI:
- Swallowing disorders
- Constipation
- Sexual/GU:
- ED + anorgasmia
- Retention
- Incontinence
- Lhermitte’s Sign
- Neck flexion → electric shocks in trunk/limbs
MS; Optic neuritis
pain on eye movement, rapid ↓ central vision
Uhthoff’s: vision ↓ c¯ heat: hot bath, hot meal, exercise
o/e: ↓ acuity, ↓ colour vision, white disc, central scotoma, RAPD
MS
INO / ataxic nystagmus / conjugate gaze palsy
- Disruption of MLF connecting CN6 to CN3
- Weak adduction of ipsilateral eye
- Nystagmus of contralateral eye
- Convergence preserved
MS Viva Ix
- MRI: Gd-enhancing or T2 hyper-intense plaques
- Gd-enhancement = active inflammation
- Typically located in periventricular white matter
- LP: IgG oligoclonal bands (not present in serum)
- Abs
- Anti-MBP
- NMO-IgG: highly specific for Devic’s syn.
- Evoked potentials: delayed auditory, visual and sensory
MS viva
Ddx
Inflammatory conditions may mimic MS plaques:
- CNS sarcoidosis
- SLE
- Devic’s: Neuromyelitis optica (NMO)
- MS variant c¯ transverse myelitis and optic atrophy
- Distinguished by presence of NMO-IgG Abs
MS viva
Mx acute attack
Methylpred 1g IV/PO /24h for 3d
- Doesn’t influence long-term outcome
- ↓ duration and severity of attacks
MS viva
Mx Prevent relapse
- Preventing Relapse: Disease Modifying
- IFN-β: ↓ relapses by 30% in RRMS MS
- Glatiramer: similar efficacy to IFN-β
- Preventing Relapse: Biologicals
- Natalizumab: anti-VLA-4 Ab
- ↓ Relapses by 2/3 in RRMS
- Alemtuzumab (Campath): anti-CD52
- 2nd line in RRMS
- Natalizumab: anti-VLA-4 Ab
MS viva
Mx Symptoms: Fatigue Depression Pain Spasticity Urgency / frequency ED Tremor
Fatigue: modafinil
Depression: SSRI (citalopram)
Pain: amitryptylline, gabapentin
Spasticity: physio, baclofen, dantrolene, botulinum
Urgency / frequency: oxybutynin, tolterodine
ED: sildenafil
Tremor: clonazepam
MS viva
poor prognosis
- Older female
- Motor signs @ onset
- Many relapses early on
- Many MRI lesions
MND Examination
I TPR S Completion
- Inspection
- Wasting and fasciculation
- Esp. tongue fasciculation
- Wasting and fasciculation
- Tone
- Spastic
- Power
- Weak
- Reflexes
- Absent and/or brisk
- E.g. absent knee jerks c¯ extensor plantars
- Absent and/or brisk
- Sensation: NORMAL
- Completion
- Speech
- Bulbar: nasal
- Pseudobulbar: hot-potato
- Jaw-jerk
- Bulbar: absent
- Pseudo-bulbar: brisk
- Speech
- Eye movements: MND does not involve the eyes
MND viva
Ddx
- Cervical cord compression → myelopathy
- Brainstem lesions
- Polio: asymmetrical LMN paralysis
- Mixed UMN and LMN Signs
- MND
- Ataxia, Friedrich’s
- SCDC: B12
- Taboparesis
Viva
mixedUMN/LMN signs Ddx
Mixed UMN and LMN Signs (MAST)
- MND
- Ataxia, Friedrich’s
- SCDC: B12
- Taboparesis