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Neurology Review

Omar K.
MRCP Ireland
2015
Cerebral arteries
• Anterior cerebral artery: cause a weak, numb
contralateral leg ± similar, if milder, arm
symptoms. The face is spared.
• Middle cerebral artery cause contralateral
hemiparesis, hemisensory loss (esp. face & arm),
contralateral homonymous hemianopia.
• Posterior cerebral artery: Supplies the occipital
lobe. Occlusion gives contralateral homon
ymous hemianopia (often with macula sparing).
brain stem
• lateral medullary syndrome, in which
occlusion of the posterior inferior cerebellar
artery (PICA) causes infarction of the lateral
medulla ( vertigo, vomiting, dysphagia,
nystagmus, ipsilateral ataxia, soft palate
paralysis, ipsilateral Horner’s syndrome, and a
crossed pattern sensory loss—analgesia to
pinprick on ipsilateral face and contralateral
trunk and limbs).
Headache
• Giant cell arteritis: >50yrs old with a headache
that haslasted a few weeks. Tender, thickened,
pulseless temporal arteries; jaw claudication;
• ESR >40mm/h. Prompt diagnosis and steroids
avoid blindness.
Cluster headache
• Pain is strictly unilateral and almost always
affects the same side. It lasts 15–160min, occurs
once or twice a day, and is often nocturnal. (2am)
• Tx : 100% O2 for ~15min via non-rebreathable
mask (not if COPD); sumatriptan (anti migraine)
• Prevention verapamil 360mg, lithium 900mg, and
melatonin 10mg.
Trigeminal neuralgia
• Paroxysms of intense, stabbing pain, lasting seconds, in the trigeminal nerve
distribution. It is unilateral, typically aff ecting mandibular or maxillary
divisions.
• . Triggers: Washing affected area, shaving, eating, talking, dental prostheses

• Tx
• 1_Carbamazepine (start at 100mg/12h PO; max 400mg/6h; lamotrigine;
phenytoin 200–400mg/24h PO; or gabapentin (p508). If drugs fail,
• 2_surgery may be necessary. This may be directed at the peripheral nerve,
the trigeminal ganglion or the nerve root.
• A_Microvascular decompression: Anomalous vessels are separated from
the trigeminal root.
• B_Stereotacticgamma knife surgery can work, but length of pain relief and
the time to treatment response are limiting factors
Migraine =misery
• Visual or other aura (see below) lasting 15–
30min followed within 1h by unilateral,
throbbing headache. Or:
• •Isolated aura with no headache;
• •Episodic severe headaches without aura, often
premenstrual, usually unilateral, with nausea,
vomiting ± photophobia/phono phobia
(‘common migraine’).
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• Partial triggers Seen in 50%: CHOCOLATE or:
chocolate, hangovers, orgasms,
• cheese, oral contraceptives, lie-ins, alcohol,
tumult, or exercise.
tx
• NSAIDS (eg ketoprofen 100mg, dispersible aspirin
900mg/6h)
• Triptans (CI IHD, coronary spasm, uncontrolled BP,)
• Cafergot, sumatriptan

• Prevention Remove triggers


• 1st-line: Propranolol 40–120mg/12h, amitriptyline 10–
75mg nocte, Ca2+ channel blockers
• 2nd-line: Valproate, gabapentine
Blackouts
• Stokes–Adams attacks Transient arrhythmias (eg
bradycardia due to complete heart block) causing reduced
cardiac output and LOC.

• The patient falls to the ground (often with no warning


except palpitations), pale, with a slow or absent pulse.
• Recovery is in seconds, the patient flushes, the pulse
speeds up, and consciousness is regained.
• Injury is typical of these intermittent arrhythmias. .
Attacks may happen several times a day and in any posture
Vertigo
• An illusion of movement
Acoustic neuroma
• It often presents with unilateral hearing loss,
with vertigo occurring later.
• With progression, ipsilateral Vth, VIth, IXth, &
Xth nerves may be affected (also ipsilateral
cerebellar signs).
Paradoxically, the VIIth nerve is rarely.

5.6.7.8.9
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Hearing loss
• Rinne Rinne positive: AC > BC,
• SNAC–RIP’:in sensorineural loss and normal
ears, air conduction is better—Rinne is positive.

• Weber: ask the patient which ear the sound is


heard in. Sound localizes to the affected ear with
conductive loss (>10dB loss),
• to the contralateral ear in SNH
tremors
• • Rest tremor: abolished on voluntary movement. Cause:
parkinsonism.
• • Intention tremor: irregular, large-amplitude, worse at the
end of purposeful acts, eg fi nger-pointing or using a
remote control. Cause: cerebellar damage (eg MS, stroke).
• • Postural tremor: absent at rest, present on maintained
posture (arms out stretched) and may persist (but is not
worse) on movement. Causes: Benign essential tremor
(autosomal dominant; improves with alcohol),
thyrotoxicosis, anxiety, b2-agonists
CVA
• CI •
• Major infarct or haemorrhage on CT •
• Mild/non-disabling deficit •
• Recent birth,surgery, trauma, or artery or vein puncture at
uncompressible site •
• Past CNS bleed • AVM or aneurysm •
• Severe liver disease, varices or portal hypertension
• Seizures at presentation •
• Anticoagulants or INR >1 . 7 • Platelets <100 ≈ 109/L • BP
>220/130
TIA
• What to do ? & WHY
Subarachnoid haemorrhage (SAH)
• devastating typically occipital headache—“I thought I’d been kicked in the
head”.
• Vomiting, collapse, seizures and coma often. 
• Mx

• 1_Refer all proven SAH to neurosurgery immediately.


• 2_Maintain cerebral perfusion by keeping well hydrated, and aim for SBP
160mmHg. Treat BP only if very severe.
• 3_ Nimodipine (60mg/4h PO for 3wks, or 1mg/h IVI) is a Ca2+ antagonist
that reduces vasospasm and consequent morbidity from cerebral ischaemia.
• 4_Endovascular coiling is preferred to surgical clipping where possible
Microcatheters can now traverse tortuous vessels to treat previously
• unreachable lesions.
Intracranial venous thrombosis
(IVT)
• Invx MRI/MRV !!!!!!!!
• Causes ???

• Mx
• 1_ good hydration
• 2_Thrombolytic Therapy
• 3_large parenchymal lesions
• causing herniation,
• decompressive surgery has been
• lifesaving
Subdural vs extradural
• SUB D . Fluctuation GSC
• CT scan :crescent-shaped collection of blood over 1
hemisphere

• Ext dural :conscious level falls or is slow to improve,


or there is a lucid interval
• CT biconvex/lens-shaped

• NP :LP at ALLLLLLLLLLLLLLLLLLLLL
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Dementia
• syndrome encompassing progressive defi cits
in several cognitive domains. The initial
presentation is usually
• of memory loss
• over months or years.
tx
• Treat every thing
1_Acetylcholinesterase inhibitors
• Donepezil:
• Rivastigmine:
• Galantamine:
2_Antiglutamatergic :memantine
Seizure /epilepsy /convulsion
• Causes
• Types

• mx
Parkinsonism
• TRAP
• Medication
1_Tremors : Anticholinergic (benzhexol)
2_Rigidty & bradykinesia :
• Early Dopamine agonists (DA):Ropinirole
• Late levodopa
• 3_On/oFF COMT inhibitors entacapone
Multiple sclerosis (MS)
• plaques of demyelination occur at multiple CNS sites
(versions)
• Mainly eyes (optic neurtitis )

• DX mcdonald criteria
• Tx
• 1_happy life (hummmmmmmmm)
• 2_steroids
3_interferon (1a ,1b)
• 4_MAB
Idiopathic intracranial hypertension
(=pseudotumour cerebri)
• (headache, ICP and papilloedema) = ?

• Invx

• Tx Weight loss, acetazolamide, loop diuretics,


and prednisolone
Bell’s palsy
• UMNL VS LMNL

• Tx

• Steroids & acyclovir


PNP
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Tests Tests FBC, ESR, glucose, U&E, LFT, TSH, B12,


electrophoresis, ANA & ANCA (p555), CXR,
urinalysis, and consider an LP ―
Autonomic neuropathy
• DM, amyloidosis, Guillain–Barré and Sjögren’s syndrome,
HIV, leprosy, SLE,
• toxic, genetic (eg porphyria), or paraneoplastic,
• neuropathies and Lambert–Eaton myasthenic syndrome
(LEMS).
Signs:
• 1_Postural hypotensions
• 2_erectile dysfunction
• 3_sweatings,
• 4_constipation, nocturnal diarrhoea, urine retention,
invx
Autonomic function tests
1_• Postural drop of 20/10mmHg is abnormal. :
p39.
2_• ECG: A variation of <10bpm with respiration is
abnormal.
3_• Cystometry: Bladder pressure studies.
4_• Pupils:
5_ Paraneoplastic antibodies: Anti-Hu, anti-Yo, anti-
Ri,
Motor neuron disease (MND)
• selective loss of neurons in motor cortex, or cranial nerve nuclei, and anterior
horn cells. Upper and lower motor neurons are affected but there is no
sensory loss or sphincter disturbance VS MS.

Types
• ALS/amyotrophic lateral sclerosis UMN signs + LMN
wasting/fasciculationting.
• Progressive bulbar palsy (10%) Only affects cranial nerves IX–XII. UMNL
• 3 Progressive muscular atrophy (10%) Anterior horn cell lesion only, thus
no UMN signs. Affects distal muscle groups before proximal.

• 4 Primary lateral sclerosis thus mainly UMN signs + marked spastic leg
weakness and pseudobulbar palsy
invx
• MRI + CT TRO other conditions
• Dx is clinica l
• Tx Antiglutamatergic drugs: Riluzole (BOX)
prolongs life by ~3 months 
Signs of cord compression:
• • Spastic leg weakness (often 1 leg > other)
• • Weak, clumsy hands
• • Numbness in hands
• • ‘Heavy’ legs
• • Foot-drop/poor walking
• • Incontinence, hesitancy & urgency are often
late341
Primary disorders of muscle (myopathies)

• Muscular dystrophies are a group of genetic


diseases with progressive degeneration and
weakness of specific muscle groups.

• Duchene & Becker’s muscular dystrophy


• FSHD
Myasthenia gravis (MG)
antibodies to nicotinic acetylcholine receptors
• (AChR), at post-synaptic receptor sites
• Tests
• Antibodies: Anti-AChR antibodies in 90%; if sero
negative look for MuSK antibodies (muscle specifi c
tyrosine kinase)
• • Neurophysiology: Decremental muscle response
to repetitive nerve stimulation ± single-fibre jitter. •
Imaging: CT of thymus.
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• 1_Symptom control Anticholinesterase, eg pyridostigmine.
Cholinergic SE: salivation, lacrimation, sweats, vomiting, miosis.
Other SE: diarrhoea, colic
• 2_Immunosuppression: Treat relapses with prednisolone—start at
5mg on alternate days,  by 5mg/wk up to 1mg/kg on each
treatment day. dose on remission (may take months). Give osteo
porosis prophylaxis. SE: weakness (hence low starting dose).
• Steroids may be combined with azathioprine weekly
methotrexate.IV methylprednisolone has a role.
• Thymectomy: Expect remission in 25% and worthwhile benefi t in
• a further 50%.
Lambert–Eaton myasthenic syndrome

• Antibody to the pre-synaptic membrane’s


voltage-gated Ca2+ channels
• paraneoplastic (from small-cell lung cancer)
tests
• 1_anti VGCC antibodies are +ve in 85%).
• 2_Electrical post-tetanic potentiation with
>60%  in post-exercise increament vs MG
• Tx 3,4-diaminopyridine or IV immunoglobulin
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Syringomyelia
• Dissociated sensory loss (absent pain and T°
sensation, with preserved light touch, vibration,
and joint-position sense) due to pressure from
the syrinx on the decussating antero lateral
pathway in a root dis tribution refl ecting the
location of the syrinx (eg for typical cervical
syrinx then sensory loss is over trunk and
arms); wasting/weakness of hands ± claw-hand
Sensory
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motor
• Same level LMNL

• Below it UMNL
Brown sequard lesion
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