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NEUROLOGY
NERVOUS SYSTEM STRUCTURE & FUNCTION
Areas of the brain ...................................................................86
Vision ...............................................................................................87
Spinal cord tracts ....................................................................88
NERVOUS SYSTEM INVESTIGATIONS
Lumbar puncture ....................................................................90
Imaging with CT & MRI .......................................................91
ACUTE NEUROLOGICAL DISEASE
Acute spinal problems ........................................................92
Neuromuscular emergencies .........................................93
Acute hydrocephalus ...........................................................94
Cortical venous sinus thrombosis ...............................95
Stroke and cerebrovascular disease .........................96
07
CNS infection .............................................................................99
Brain abscess ..........................................................................100
LONG-TERM NEUROLOGICAL CONDITIONS
Neuro-oncology .................................................................... 101
Multiple sclerosis ................................................................. 102
Epilepsy ...................................................................................... 104
Neuropathies .......................................................................... 107
Motor neurone disease ...................................................110
Myasthenia gravis ...............................................................111
Myopathies ..............................................................................112
Essential tremor ...................................................................113
Headaches ................................................................................ 114
ABBREVIATIONS
# – Fracture
Ab – Antibody
ACA – Anterior cerebral artery
ACh – Acetylcholine
AED – Anti-epileptic drug
APS – Antiphospholipid syndrome
BBB – Blood–brain barrier
BZD – Benzodiazepine
CBT – Cognitive behavioural therapy
CIDP – Chronic inflammatory
demyelinating polyradiculopathy
CJD – Creutzfeldt–Jakob disease
CK – Creatine kinase
CLD – Chronic liver disease
CMT – Charcot–Marie–Tooth
CMV – Cytomegalovirus
CN – Cranial nerve
CNS – Central nervous system
CSF – Cerebral spinal fluid
CTD – Connective tissue disease
CVST – Cortical venous sinus thrombosis
DCML – Dorsal column medial lemniscus
DIC – Disseminated intravascular
coagulation
EBV – Epstein–Barr virus
EEG – Electroencephalography
EID – Electronic implantable device
EMG – Electromyography
GBS – Guillain–Barré syndrome
GCA – Giant cell arteritis
GCS – Glasgow Coma Score/Scale
HNPP – Hereditary neuropathy with
pressure palsies
HSV – Herpes simplex virus
IC – Intracranial
ICA – Internal carotid artery
ICP – Intracranial pressure
ILAE – International League Against Epilepsy
IVH – Intraventricular haemorrhage
LMN – Lower motor neurone
LOC – Loss of consciousness
LP – Lumbar puncture
LSBP – Lying & standing blood pressure
MCA – Middle cerebral artery
MG – Myasthenia gravis
MND – Motor neurone disease
MS – Multiple sclerosis
N / n. – Nerve
NCS – Nerve conduction study
NMJ – Neuromuscular junction
OCP – Oral contraceptive pill
PCA – Posterior cerebral artery
PCR – Polymerase chain reaction
PNS – Peripheral nervous system
SAH – Subarachnoid haemorrhage
SAN – Spinal accessory nerve
SLE – Systemic lupus erythematosus
SOL – Space-occupying lesion
SSRI – Selective serotonin reuptake
inhibitor
TCA – Tricyclic antidepressant
TIA – Transient ischaemic attack
UMN – Upper motor neurone
VDRL – Venereal Disease Research
Laboratory
VF – Visual field
86 Chapter 7: Neurology Nervous system structure & function
Premotor
Le
Spinal cord
l
Motor
https://t.me/med1917
Areas of the brain
Language centres:
→ usually in dominant hemisphere
1. Broca’s area: expression
→ Area 44 & 45 (inferior frontal gyrus)
→ Broca’s aphasia = expressive dysphasia
(non-fluent speech)
2. Wernicke’s area: reception
→ Area 22 (superior temporal gyrus)
→ Wernicke’s aphasia = receptive dysphasia
(impaired language comprehension)
Causes of cerebellar damage: ‘PASTRIES’
P – Posterior fossa tumour
A – Alcohol
S – Multiple sclerosis
T – Trauma
R – Rare causes (neurodegenerative,
paraneoplastic)
I – Inherited (e.g. Friedreich's ataxia)
E – Epilepsy treatments
S – Stroke
Prefrontal
cortex
ft cerebral
hemisphere
Broca’s
area
Primary
auditory
cortex
cortex
Pons
Medulla
oblongata
Fig. 7.1 Surface anatomy of the brain.
cortex
Primary somatic
sensory cortex
Parietal
lobe
Gustatory
area
Wernicke’s
area
Primary visua
cortex
Optic
radiation
Cerebellum
The cerebellum
→ function: balance & coordination of ipsilateral muscles
Symptoms of cerebellar dysfunction:
• Ataxia → broad-based gait (worse when heel-to-toe walking)
• Intention tremor → absent at rest
• Upward drift → with arms straight out in front, eyes closed
• Positive rebound phenomenon
• Dysmetria → cannot estimate distance (finger-to-nose test)
• Dysarthria → slow, slurred ‘staccato’ speech (say ‘British Constitution’)
• Dysdiadochokinesia → clumsy alternating rapid movements
• Nystagmus
The brainstem
→ function: control of vital functions e.g. breathing
The cranial nerves
I Olfactory Smell
II Optic Vision
Midbrain: CN III & IV
+ Edinger–Westphal nucleus
Vertical & horizontal eye movements
III Oculomotor Eye movement
IV Trochlear Eye movement
V Trigeminal Face & anterior 2/3 tongue sensation
Chewing
Pons: CN V, VI, VII & VIII
Horizontal eye movements & facial muscles
Medulla: CN IX, X, XI & XII
+ Vestibular nuclei (between pons & medulla)
(damage = vertigo)
+ Nucleus ambiguous
(damage = swallow issues)
+ Pyramidal decussation (spinothalamic)
(contralateral pain/temperature loss)
+ Respiratory & cardiac centres
VI Abducens Eye movement
VII Facial Taste (anterior 2/3 tongue)
Facial muscles
Lacrimal & salivary glands
VIII Vestibulocochlear Balance & hearing
IX Glossopharyngeal Taste (posterior 1/3 tongue)
Gag reflex
X Vagus Auricle, diaphragm, gut sensation
Uvula & swallowing (gag reflex)
Voice muscles
GIT autonomic functions
XI SAN Trapezius (turn neck & shrug)
XII Hypoglossal Tongue movement
KEY:
Sensory function
Motor function
Autonomic function
Medicine
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Vision
Visual eld defects
1. Bitemporal hemianopia = due to lesion in optic chiasm
2. Any one-sided loss (homonymous) = retrochiasmal & will be contralateral
to lesion
3. Quadrantanopias = temporal or parietal lobe lesions → ask about other symptoms
1. Monocular blindness
Fig. 7.2 Optic pathway.
2. Bitemporal hemianopia
= chiasm lesion
Causes:
• Pituitary tumour
• Rathke’s pouch meningioma
• Craniopharyngioma (kids)
3. Homonymous hemianopia
= optic tract, optic radiation, or occipital cortex lesion
4. Superior homonymous quadrantanopia
= temporal lobe lesion
→ Inferior fibres of optic radiation affected
5. Inferior homonymous quadrantanopia
= parietal lobe lesion
→ Superior fibres of optic radiation affected
6. Homonymous hemianopia + macular sparing
= lesion of PCA but spared MCA
Extra-ocular muscles:
SR – superior rectus
MR – medial rectus
IO – inferior oblique
1
2
3
5
6
4
IR – inferior rectus
LR – lateral rectus
SO – superior oblique
1
2
3
4
5
6
Eye muscle palsies
3rd nerve palsy 4th nerve palsy 6th nerve palsy
Symptoms/signs • Ptosis – levator palpebrae
• Down & out – SR, IR, MR, IO
• Efferent pupil defect – dilated
Causes Pupil sparing: stroke*, microvascular
events, demyelination
Non-pupil sparing: tumour, orbital
• Up & in – SO
• Compensatory head tilt
away from affected eye
Trauma = most common
(+ other causes same as
3rd nerve palsy)
trauma, PCA aneurysm
*3rd nerve palsy due to stroke is usually
accompanied by other symptoms
Appearance
Horner’s syndrome
→ arises due to disruption of sympathetic oculomotor supply to the eye
SYMPTOMS:
• Unilateral miosis
(pupil constriction)
• Partial ptosis
• Anhidrosis
• Apparent exophthalmos
CAUSES:
Brainstem: tumour, medullary stroke,
MS, basal meningitis
Intrathoracic lesion: Pancoast tumour,
cervical rib
Neck lesion: lymphadenopathy,
trauma, thyroid surgery
Intracranial: ICA aneurysm, migraine
• Adducted – LR
Trauma, tumour, demyelination,
stroke*, microvascular events,
idiopathic intracranial hypertension*
*6th nerve palsy can be a falsely
localising sign of ICP
Medicine
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Spinal cord tracts
The descending spinal tracts
Corticobulbar tract innervates each cranial
nerve bilaterally except for:
Pyramidal tracts = voluntary control (cerebral cortex → brainstem & spinal cord)
1. Facial nerve (CN VII):
→ Forehead = bilateral representation
→ Branch to lower face = unilateral
representation
→ UMN lesion spares frontalis
2. Hypoglossal (CN XII):
→ Each half of tongue supplied by contralateral
corticobulbar tract
→ Lesion causes contralateral weakness, so
tongue deviates towards weak side
UMNs
Cerebral
cortex
Brainstem
Spinal
cord
Fig. 7.3 Pathway of UMNs & LMNs.
*Pyramidal weakness:
Upper limbs: extensor muscles weaker than
flexors
= results in flexed elbow & wrist
Lower limbs: flexor muscles weaker than
extensors
= results in extended knee/ straight leg
Cranial n.
Spinal n.
LMNs
Head & Neck
muscles
Limb
muscles
Corticospinal: voluntary movement of
contralateral body
→ Originate in motor cortex
→ Decussate in medullary pyramids
→ Synapse with LMNs in spinal cord
Corticobulbar: voluntary movement of face &
neck
→ Originate in motor cortex
→ Terminates in brainstem
→ Synapse with cranial nerves
The ascending tracts
Dorsal column medial
lemniscus (DCML)
Fine touch, vibration,
proprioception
(contralateral)
Spinothalamic Spinocerebellar
Pain & temperature
(contralateral)
Unconscious proprioception (ipsilateral)
(awareness of position & movement of
body parts in space without conscious
thought)
Upper motor neurones vs. lower motor neurone lesions
UMNs: motor cortex → internal capsule → brainstem → spinal cord
LMNs: anterior horn cell → nerve root → peripheral nerve → NMJ → muscle
Upper motor neurone lesion
(brain + spinal cord)
Signs • Hypertonia
• Hyper-reflexia
• Pyramidal weakness*
• Clonus
• +ve Babinski
• Spastic gait
Causes • Stroke / brain tumour
• Spinal tumour / injury
• Cerebral palsy / MS
Lower motor neurone lesion
(peripheral nerves)
• Hypotonia
• Hypo-reflexia
• Proximal/distal weakness
• Wasting
• Fasciculations
• Peripheral neuropathy (DM, alcohol, drugs)
• Polio (anterior horn cells) / Guillain–Barré
• MND
• Myasthenia gravis
Facial weakness
Bulbar palsy: LMN lesion causing dysarthria
= weakness of muscles supplied by CN IX, X, XII
→ Nasal speech / dysarthria
→ Hyporeflexia: jaw jerk & gag reflex absent
→ Tongue: weak & wasted & fasciculations
Medicine
Upper motor neurone lesion Lower motor neurone lesion
Signs • Contralateral weakness
• Frontalis spared
Causes • Stroke / brain tumour
• Subdural haematoma
• MS
Pseudobulbar palsy: bilateral UMN lesion causing dysarthria = damage to medullary
cranial nerves
→ ‘Donald Duck’ speech (spastic dysarthria)
→ Hyperreflexia: jaw jerk & gag reflex increased
→ Tongue: weak & spastic
• Ipsilateral weakness
• Whole face
• Bell’s palsy
• GBS (usually bilateral)
• Infection (HSV, CMV, EBV, Lyme disease)
• Trauma
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Dermatomes
C4
T2
C5
T1
Fig. 7.4
Myotomes
Nerve root Motor function
L1
L1
S2
L2
L3
C6
L5
L4
C8
C7
S1
S5
L2
S3
S4
S2
L5
L4
S1
C5 Elbow flexion
C6 Wrist extension
C7 Wrist flexion, finger extension, elbow extension
C8 Finger flexion
T1 Finger abduction
L1,2 Hip flexion
L3 Knee extension
L4 Ankle dorsiflexion
L5 Knee flexion, big toe extension
S1 Knee flexion, ankle plantarflexion, big toe flexion
Deep tendon reflex Nerve roots
Biceps + brachioradialis C5, C6
Triceps C7, C8
Knee jerk L3, L4
Ankle jerk S1, S2
Focal peripheral nerve lesions
Lesion Symptoms Sensory loss Motor loss Causes
Median nerve
(C5–T1)
Carpal tunnel
Ulnar nerve
(C8–T1)
Cubital tunnel
Radial nerve
(C5–T1)
Brachial plexus
(C4–T1)
Axillary nerve
(C5–C6)
Common
peroneal nerve
(L4–S2)
• Pain/tingling in
hand
• Thenar muscle
wasting
Dorsal & palmar aspect
of lateral 3.5 digits
• Middle & index fingers (L)
• Thenar muscles (OAF)
Lumbricals
Opponens
• Repetitive motion
• DM/thyroid
• RA/OA
• Pregnancy
Abductor pollicis brevis
Flexor opponens
• Pain/tingling in
hand
• Weak grip
• Ulnar claw
(paradox)
Dorsal & palmar aspect
of medial 1.5 digits
All small hand movement except LOAF
(interossei/lumbricals)
• Finger abduction & adduction
• Thumb adduction
• Little & ring finger flexion
• Elbow trauma
• Idiopathic
• Wrist flexion
• Wrist drop Dorsal hand & 1st web
space
• Erb’s palsy
Shoulder & arm Deltoid, biceps, brachialis, rotator cuff,
(weakness,
sensory loss &
muscle atrophy)
Brachioradialis: Wrist extension
Extensor digitorum: Finger extension
serratus anterior
• Humerus fracture
• Idiopathic
• Trauma
• Damage from assisted delivery at birth
• Compression
• Inflammatory
• Deltoid wasting Regimental badge area Deltoid: shoulder abduction • Proximal humerus fracture
• Foot drop Lateral calf & dorsum
of foot
Tibialis anterior: dorsiflexion & eversion • Sporting injury
(direct trauma near knee)
• Fibular head fracture
• Habitual leg crossing
Medicine
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Lumbar puncture
Method
1. POSITION PATIENT
→ Ideal position = lateral decubitus
Patient lies on their side, curled forwards with their knees towards their chest to
open the lumbar interspinous spaces. This is the only way opening pressure
can be measured.
Layers through which the needle passes:
Skin → Subcutaneous tissue → Ligamentum
flavum → Subarachnoid space
→ If cannot lie on side / obese (or opening pressure not needed)
Patient sits up, and curls forwards over a pillow.
→ Cannot assess opening pressure if patient in sitting position
2. FIND PUNCTURE SITE: L3/L4 or L4/L5 spaces
• Identify L4 spine – palpate tops of the iliac crests & L4 is halfway between
(along line of the intercristal plane)
• LP needle inserted obliquely above L4 – parallel to plane of the spine
through the interspinous ligament
Indications for LP:
1. Diagnosis of:
• Infection e.g. meningitis,
encephalitis
• Neurodegeneration e.g. CJD
• Inflammation e.g. MS, GBS
• SAH (if clinically suspected but no
evidence on CT)
2. Measurement of CSF pressure
(if no contraindication)
3. Therapeutic removal of CSF
4. Intrathecal drug administration
Possible complications of LP
Common Rare
• Low pressure headache (30%)
→ worse when sitting up, better lying flat
→ typically resolves by 2w
→ treat with analgesics ± blood patch
• Backache (30%)
• Pain of anaesthetic & puncture
• Dr y tap / unsuccessful procedure
• Infection
• Serious bleeding e.g. epidural haematoma
• Damage to spinal nerves / lasting neuro deficit
• Coning of the cerebellar tonsils / death
Contraindications for LP:
1. Suspected raised ICP: will cause
coning & death
e.g. posterior mass lesion, ventricular
obstruction
Signs: papilloedema, focal neuro
deficit / seizures
2. Increased bleeding risk:
• Anticoagulants – stop before LP
• Thrombocytopenia (platelets <50)
• Thrombophilias (INR >1.5)
3. Intracranial abscess / severe septic
features / meningococcal rash
→ never do if suspect ICP due to SOL
Medicine
Causes of raised opening pressure
→ Bacterial/viral infection
→ Cerebral haemorrhage
→ Idiopathic intracranial hypertension (pressure >25cmH2O)
→ Venous sinus thrombosis
normal opening pressure <25cmH2O
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Imaging with CT & MRI
Common indications for brain imaging
• Trauma
• Tumour
• Stroke/TIA
• Neurodegeneration
• Inflammation
• Infection
CT versus MRI
CT scan MRI scan
Advantages • Quick, readily available
• Very sensitive for haemorrhage
Disadvantages • Ionising radiation
• Not as detailed as MRI
• Not if pregnant
Indications In acute setting (quick):
• assessment for early thrombolysis
• very sensitive for IC haemorrhage
Patients who present with:
• Headache
• Vomiting
• Fever
• Seizure
Head trauma plus: ‘panda eyes’ / anticoagulated /
vomiting / seizures
• Non-ionising
• More detailed image / detects
• Safe in pregnancy after 1st trimester
• Contraindications: metal implants /
• Takes longer / less available
• More expensive
• Small/subtle infarcts
• Posterior fossa assessment
• MS, epilepsy, tumours
• Low GCS / altered
behaviour
• Focal neurology
inflammation
EIDs / claustrophobia
CT imaging of intracranial haemorrhage
Epidural/extradural haematoma
Arterial blood (middle meningeal artery)
Between skull & outer layer of dura Between dura & arachnoid mater Between arachnoid membrane & pia mater
Sx: lucid interval → unconscious
Fig. 7.5
• Lentiform / bi-convex shaped
• Does not cross suture zones (confined)
• Midline shift
Other neurological investigations
Nerve conduction studies (electromyography – EMG)
Indications:
• Polyneuropathy of unknown cause
• Mononeuritis multiplex
• Mononeuropathy that cannot be localised clinically
• Neuromuscular junction disorders / muscular disease
• Anterior horn cell disorders (e.g. MND)
Subdural haematoma
Venous blood (bridging veins)
Sx: progressive headache & confusion Sx: thunderclap headache
Fig. 7.6
• Crescent-shaped
• Crosses suture lines
• Midline shift
Electroencephalography (EEG)
Indications:
• Seizures → determine type/diagnosis of epilepsy
• Assess for encephalitis
Subarachnoid haemorrhage
Fig. 7.7
• Linear/star-shaped
• Within sulci
Medicine
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Acute spinal problems
Acute cauda equina syndrome
→ BILATERAL sciatica
→ Saddle anaesthesia (S2, S3, S4)
→ Bladder/bowel incontinence
= emergency referral for MRI scan
Common cause:
→ central lumbar disc herniation
Cord compression
Symptoms can develop over a few hours:
→ Increasing thoracic back pain & local tenderness
→ Increasing leg weakness & incontinence
Management:
→ Urgent neurosurgical referral
→ MRI spine
Important cause: metastases
→ from breast, prostate, lung,
thyroid, renal, bowel
Acute spinal stroke
Pathogenesis: ischaemia or haemorrhage affecting vascular supply to spinal cord
Symptoms: (appear suddenly)
→ Severe neck/back pain
→ Leg weakness
→ Altered sensation
→ Bladder/bowel incontinence
Management:
→ MRI spine + stroke management
Transverse myelitis
Pathogenesis: inflammation of spinal cord
Causes: idiopathic, autoimmune (MS), infection, systemic inflammatory (SLE)
Investigation: CSF analysis, antibody testing, spinal cord imaging
Acute injury/compression of the spinal cord
1. Initial spinal shock = flaccid areflexia & paralysis, hypotension & bradycardia
2. Development of UMN signs: spasticity, hyperreflexia, increased tone etc.
Medicine
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Neuromuscular emergencies
→ Arise when weakness affects respiratory or bulbar muscle function
→ Can lead to type 2 respiratory failure
Underlying causes
neuromuscular emergencies may be precipitated by
infection
1. ACUTE: Guillain–Barré, myasthenic crisis
Blood gas → high CO2 + low pH & bicarbonate = respiratory acidosis
(no time for compensation)
2. CHRONIC: MND, myotonic dystrophy, chronic myopathies
Blood gas → high CO2 + normal pH & high bicarbonate
(body compensates for respiratory acidosis over time)
Clinical presentation of acute cases
• Weak diaphragm = breathless (especially when flat), accessory muscle use,
paradoxical diaphragm movement
• Weak intercostal/abdominal muscles = weak cough
• Weak bulbar muscles = cannot clear secretions, weak facial muscles
• Signs of progressive hypercapnia & hypoxia = tachycardia, sweating,
flap → confusion
Assessment
• FORCED VITAL CAPACITY = best predictor of need for HDU
▶ In 70kg person, <1.5L = serious concern
▶ Drop of >20% from upright → supine = diaphragm paralysis
• General obs: HR & RR
• ABG: respiratory acidosis
• Neuro assessment: weak limbs, face & swallow (cannot complete sentences /
count from 1 to 20)
ABG RESULTS
Acute T2RF Chronic T2RF
→ O2 <8kPa
→ CO2 >6kPa
→ pH <7.35
→ Bicarb = low/
normal
NB: Vital capacity normally decreases
by 10% from upright → supine
→ O2 <8kPa
→ CO2 >6kPa
→ pH = normal
→ Bicarb = >26mmol/L
Management
1. Call for help (anaesthetist & ICU)
2. Secure airway: sit up, O2 if <94%, suction secretions, NBM
3. IV access: bloods & blood gases
4. CXR: for infection (common trigger)
5. Neurology / critical care input for further management
Medicine
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Acute hydrocephalus
Accumulation of CSF within ventricles causing dilation & raised ICP
Types
1. Communicating (non-obstructive): impaired CSF absorption → post-
infection (TB), SAH, haemorrhagic stroke
2. Non-communicating (obstructive): blocked CSF flow between ventricles =
drainage → tumours
Causes of congenital hydrocephalus
• Genetic abnormality
• Developmental abnormality of brain/SC/spine
• Premature complications (IVH)
• Infection during pregnancy (e.g. rubella)
Risk factors for acute hydrocephalus:
• Congenital malformation of ventricular
system
• Posterior fossa / brainstem tumours
• Post brain injury (SAH, meningitis, trauma)
Normal pressure hydrocephalus:
Symptoms
• Headache, N&V
• Blurred vision, papilloedema
• Ataxia (poor balance)
• Altered consciousness / sleepy
• Altered personality / irritable
→ bilateral UMN signs due to corticospinal tract disruption
Investigations
• CT/MRI head
• Lumbar puncture
Management
1. Surgical:
• Shunt insertion
• Endoscopic third ventriculostomy (ETV)
• ± removal of obstruction if present
2. Rehab: physio, OT, psychology
Raised intracranial pressure (>25mmHg)
= dilated ventricles with normal ICP (slow
increase in CSF, allowing surrounding tissue
to compensate so no ICP)
Presentation:
TRIAD: ataxia, incontinence, cognitive difficulties
(DDx: Alzheimer’s)
Medicine
Clinical presentation:
1. Headache of ICP
→ new onset, progressive severity
& frequency
→ associates with N&V
→ wakes patient early morning
→ worse with bending, coughing
& exertion
2. Vision changes:
→ pupil constriction (later dilation)
→ reduced acuity & visual field loss
→ papilloedema
→ may have fixed, dilated pupil (3rd CN)
3. Altered GCS: irritability, drowsiness
4. Cushing reflex (due to coning):
hypertension, bradycardia, Kussmaul breathing
Investigations:
• Hx & examination
• FBC, U&Es, LFT, glucose, clotting
• Blood culture
• CT head
• LP – only if safe (opening pressure <25)
Causes:
• Brain tumour
• Haemorrhage
• Hydrocephalus
• Status epilepticus
Complications:
• Brain herniation (coning)
• Ataxia
• CN palsies (esp. 3rd & 6th nerve)
• Irregular breathing / apnoea
• Hemiparesis
• Seizure/stroke/coma
• Infarction
Management: urgent neurosurgery
(craniotomy / burr hole)
+ ABCDE (O2, temp control)
+ seizure control
+ mannitol / hypertonic saline
• Head injury
• Brain infection/
abscess
• Cerebral oedema
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