Neurological disorders

Bell’s palsy – idiopathic facial nerve palsy

Incidence: 15–40/100,000/yr. (~1 patient/2yrs/GP).
Facial Palsy- upper or lower motor
neuron lesion that causes weakness or
♂≈ ♀.
paralysis of the facial muscles and Risk:  in pregnancy (X3) and in diabetes (X5).
symptoms associated with diminished
innervation of the facial nerve

Clinical features
- Complete unilateral facial
weakness at 24-72h
- Ipsilateral numbness or pain
around the ear
- taste
- Hypersensitivity to sounds
- Headache, facial swelling
On examination
- Patient is unable to wrinkle their
forehead
- Unilateral sagging of the mouth
- Drooling saliva
- Failure of eye closure may cause
a watery or dry eye

Test Rule out other causes.

Blood: ESR, Glucose, Borrelia antibodies in Lyme disease,  VZV antibodies
in Ramsay Hunt syndrome.
CT/MRI: Space Occupying lesions, Stroke, MS,
CSF: Rarely done for infections

Prognosis Incomplete paralysis: without axonal degeneration usually recovers completely

within a few week
Complete paralysis
Synkinesis: e.g. eye blinking causes synchronous upturning of the mouth,
misconnection of parasympathetic fibres can produce Crocodile tears (Gusto-
lacrimal reflux) when eating stimulates unilateral lacrimation not salivation

Management 1. Offer reassurance

- Patients should be reassured that most people recover from Bell palsy in
6-9 months
- Only a small number are left5 with permanent effects
2. Provide eye care
- Adequate eye lubrication with eye drops, dark glasses, artificial eye
drops
- Taping the eye to protect it, particularly during sleep
3. Prescribe prednisolone
- With 72 hours of symptoms onset
- 25mg BD for 10 days
 Guillain-Barre syndrome (acute IDP)
Pathology  Guillian-Barre syndrome refers to an immune mediated demyelinating neuropathy
- Clinically defined syndrome characterised by motor difficulty, absence of deep tendon reflexes,
paraesthesias without objective sensory loss, and increased CSF albumin with absence of cellular
reaction (albuminocytological dissociation).
- This condition is characterised by an immune-mediated attack on myelin sheath or Schwann cells of
sensory and motor nerves. This is due to cellular and humoral immune mechanisms, frequently
triggered by an antecedent infection.
- Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) is the most commonly
encountered variant.
Classification
GBS is classified according to symptoms and is divided into axonal and demyelinating forms.
 Sensory and motor: acute inflammatory demyelinating polyradiculoneuropathy (AIDP; most common)
or acute motor-sensory axonal neuropathy (AMSAN).
 Motor: acute motor demyelinating neuropathy (AMDN) or acute motor axonal neuropathy (AMAN)
 Miller-Fisher syndrome: ophthalmoplegia, ataxia, and areflexia (descending paralysis) (also
referred to as Fisher's syndrome).
 Bickerstaff's brainstem encephalitis (BBE): similar to Miller-Fisher syndrome but also includes altered
consciousness (encephalopathy) or long tract signs (hyperreflexia).
 Pharyngeal-cervical-brachial: acute arm weakness, swallowing Dx
dysfunction, and facial weakness. Diagnosis is clinical
 Acute pandysautonomia: diarrhoea, vomiting, dizziness, abdominal - Pulmonary Function tests
pain, ileus, orthostatic hypotension and urinary retention, bilateral - If diagnosis is unclear –
tonic pupils, fluctuating heart rate, decreased sweating, salivation, Further testing with anti-
and lacrimation. ganglioside antibodies or
 Pure sensory: acute sensory loss, sensory ataxia, and areflexia but GQ1B to help diagnose
no motor involvement Miller-Fisher

Clinical features
- Weakness
o Symmetrical, bilateral, ascending
weakness and paralysis
o Generally, does not progress after 4 Management
wks 1. Arrange intravenous
- Sensory Disturbances immunoglobulin/Plasma exchange
o Paraesthesia in distal extremities 2. Symptoms support – intubation (breathing
o Reduced or absent reflexes support
- Pain – back pain, limb pain or
neuropathic pain
- Autonomic dysfunction (E.G sweating
urinary retention)
- Respiratory Muscle paralysis
 Headache
Common presenting symptom in the world. Most likely to affect women
The international headache society 2013 categorise headaches into
 Primary
o Tension type headache
o Cluster headaches
o Migraines These two have sudden onset and may
peak at the point of maximal exertion
o Others (during an orgasm in post coital
 Stabbing headaches. You should aim to exclude
subarachnoid haemorrhages in these
 Exertional cases
 Post coital
 Valsalva
 Persistent

 Secondary
o usually has an attributable cause and is likely of greater severity such as trauma, vascular event, infection, raised
intracranial pressure, space occupying lesions
o Medication overuse headache – NICE recommends being alert to the possibility of medication overuse headache in
people whose headache developed or worsened while they were taking the following drugs
 Triptans, opioids, ergots or combination analgesic
 Paracetamol, aspirin

Cluster headaches:
Specific headache associated with intense pain coming from
within around or behind the eye.
 patient usually presents with a debilitating headache with
red watery eye with or without nasal congestion
Onset: any age, ♂: ♀> 5:1 (mostly male); common in smokers
Symptoms:
- Pain in unilateral -almost always affects the same side
- Several times a day without aura- might be nocturnal
- May last up to three hours and cause restlessness
- Rapid onset of excruciating pain around one eye – eye
becomes watery and bloodshot with lid swelling
- Lacrimation, facial flushing
- Sometimes chronic not episodic
Stepwise plan
- Dx is made clinically
- Encourage lifestyle changes – Alcohol and smoking
cessation
Acute attacks – give 100% oxygen for 15mins, Triptan sc 6mg
(suma) nasal spray.
Preventives – Corticosteroids short term. Verapamil 360mg,
Lithium 900mg
Trigeminal neuralgia
Severe disabling condition characterised by a painful
episode of sudden sharp stabbing pain in the region of the
trigeminal nerve distribution (specially V2 and V3 branches)
May occur secondary to nerve compression by arteries or
veins.
Symptoms:
- Paroxysms of intense, stabbing pain, lasting seconds in
the trigeminal nerve distribution
- Unilateral typically affecting mandibular or maxillary
divisions
Triggers
- Washing affected area, shaving, eating, talking dental
protheses
Typical Patient: female over 50-years-old
Secondary causes: Compression of the trigeminal root by
anomalous or intracranial aneurysm, tumour, meningeal
inflammation, MS, Zoster, skull base malformation (Chiari)
MRI may help exclude secondary causes
Rx:
1st line: carbamazepine 100mg/12h PO max 400mg/6h
(effective in about half the cases of trigeminal neuralgia but
has many side effects such as -dizziness, drowsiness and a
small risk of agranulocytosis. A derivative oxcarbazepine,
whilst being more expensive has fewer side effects)
2nd line: Baclofen and gabapentin
If drugs failpercutaneous radiofrequence coagulation or
Gamma knife.
Microvascular decompression -use to electric current to
dampen pain
Migraine
Path: Episodic primary headache that may present with or
without aura
Epidemiology: nearly 3x times more common in women
Aetiology: Condition is thought to be neurovascular.
Inflammation of trigeminal sensory neurons causes
increased vascular permeability and platelet activation.
This is thought to increase the sensitivity of neuronal fibres
which then interpret normal arterial flow through
meningeal arteries as painful. This is thought to account for
the “pulsatile” pain
Migraine without Aura
- General mnemonic “pound” is helpful
3 or more of the criteria
Pulsatile in nature
One day duration
Unilateral
Nausea
Disability -from work or from physical activity
Tension type headache
Path: Episodic or chronic headache related to stress
or difficulty. Classically described feeling a “tight-
band around the head”
More common in women. Bilateral not pulsatile
Stepwise plan (NICE 2012 CG150)
1. Further investigations are usually
unnecessary
2. Provide reassurance as this condition is
generally self-limiting
3. Provide first line pharmacological
management
- Paracetamol
- NSAIDS – (ibuprofen 400mg first line)
4. Prescribe medication for chronic recurrent
tension type headaches
- Tricyclic Antidepressant (amitriptyline)
- Titrate down over time
- NICE recommends acupuncture in this
case as a form of prophylaxis

Migraine without Aura: (British association for the Study

of Headache BASH guidelines)
- Diagnosis is easier; affects 1/3 migraine patients
- Typical aura – progressive, onset usually 5-50minutes
prior to the headache with hemianopic disturbances and
spreading scintillating scotoma.
- Aura may include paraesthesia and numbness of hand
and upper limbs
 Migraines may also be associated with menstruation
 Triggered by the three C’s (chocolate, coffee, and
cheese), red wine, alcohol, bright lights and the Combine
oral contraception pill.

Stepwise Mgx for Migraine

1. Acute treatment
- Combination therapy
 Oral triptan +NSAID
 Or Oral Triptan +Paracetamol
 12-17 years  nasal triptan
2. Prophylaxis
- If >2 attacks a month
- Propranolol or topiramate
- Topiramate is teratogenic
- Consider Acupuncture if medication contraindicated
- Lifestyle modification – reduce caffeine, and avoid triggers
Headache History taking Tips: According to the Oxford clinical medicine handbook

Onset Rapid onset:

 This type of headache concerning: Rule out
 SAH -Sudden onset “worst headache ever “often occipital, stiff neck, focal signs,
consciousness
 Meningitis- fever photophobia, stiff neck, purpuric rash coma. (Do a LP, start Abxs)
 Encephalitis- fever, odd behaviour, fits or reduced consciousness (do urgent CT head
and LP to look for signs of infection
 Post coital headaches
 Subacute/gradual onset headaches:
 Venous sinus thrombosis – subacute headache, papilledema
 Sinusitis- dull, constant ache over frontal or maxillary sinuses with tenderness +/- post
nasal drip. Pain worse on bending over. Ethmoid or sphenoid pain felt deep within the
root of the nose. Pain last 1-2 weeks. CT can confirm diagnosis but is rarely needed.
 Tropical illness: e.g. Malaria: travel history, Flu like illness, Typhus
 Intracranial hypotension: CSF leakage e.g. iatrogenic after lumbar puncture
Character  Tight band? think tension headache (the usual cause of bilateral non pulsatile
headache + sclap muscle tenderness)
 Throbbing/ pulsatile/ lateralizing? think Migraine (explained above)
Frequency Headaches that recur tend to be benign
 Migraine
 Cluster
 Trigeminal neuralgia
 Recurrent meningitis (Mollaret’s)- suspect if fever/meningism with each
headache (send CSF for herpes simplex PCR)
 Is there access to subarachnoid spaces via skull fracture or recurring cause of
aseptic meningitis (SLE e.g. sarcoid??)
Duration Chronic, progressive headaches can indicate: ICP- which is typically worse on
waking, lying, bending forward or coughing.
Also: vomiting, papilledema seizures, false localising signs or odd behaviour. Do
imaging to exclude a space occupying lesion and consider idiopathic intracranial
hypertension
Associated Eye pain +/- reduced vision
Features Think acute glaucoma Typically elderly, long sighted people. Constant pain
around one eye radiating to the forehead with reduced vision, visual haloes and a red
congested eye.
Jaw claudication tender with thickened, pulseless temporal arteries: Giant cell
arteritis (tender scalp over temporal arteries)  subacute headache with an ESR>40
(exclude all patients over 50 with a headache that has lasted for a few weeks)
Precipitating Head trauma: localised pain can be more generalised. It last for 2 weeks often
Causes resistant to analgesia. Do CT to exclude subdural and extradural haemorrhage
Also ask about:
 analgesia, sex, food – cheese, chocolate, coffee
Red Flags SEE BELOW !!!!
Drug history Culprits are mixed analgesics (paracetamol + codeine/opiates), ergotamine and
triptans
Common cause of episodic chronic daily headaches

Aspirin + naproxen = rebound headaches

Social history Ask about stress, recent life events
Red Flags to exclude in a Headache History
🚩🚩🚩
Multiple Sclerosis -2B
Definition: chronic mediated autoimmune demyelinating disorder of the central nervous system.
Mean age of onset: 30yrs ♂: ♀> 1:3 mostly females

Presentation
Usually monosymptomatic. Presents with unilateral optic neuritis (pain on eye movement and rapid
central vision). Corticospinal tract and bladder involvement are also common. Symptoms may worsen with
heat (exercise or a hot bath)
Visual  optic neuritis (often the FIRST Presentation)
 ophthalmoplegia (can cause diplopia)
 Bilateral internuclear ophthalmoplegia
 Relative afferent pupillary defect (Marcus Gunn pupil)
detected on a swinging light test

Sensory  Spinothalamic tract- loss of pain and temperature sensation

 Posterior column- loss of vibration, light touch and proprioception
 Root lesion- radicular pain usually in the lower thoracic abdominal area
 Trigeminal neuralgia
 Tingling, tightness, twisting, burning and tearing sensations are often
described by patients
Motor  Upper motor neuron features such as spasticity, hypertonia, hyperreflexia and
extensor plantar responses
 Transverse myelitis
Cerebellar  Ataxia
 Slurred speech
 Nystagmus
 Vertigo
Autonomic  Loss of bladder and bowel continence
 Erectile dysfunction
 Impotence
 Increased sweating
 Constipation
Others  Fatigue depression

Types of MS
1. Relapsing-remitting disease
Relapsing-remitting MS is also characterized as active or not active within a specified time frame
(e.g., 6 months, 1 year). As a guide, assessments for disease activity should be conducted at least
annually.
2. Progressive disease
Progressive disease, whether primary progressive (progressive accumulation of disability from
onset) or secondary progressive (progressive accumulation of disability after an initial relapsing
course), has four possible sub classifications taking into account the level of disability:
Diagnosis

 Clinically made my consultant neurologist with established criteria (McDonald 2010)

Clinical presentation Additional evidence needed for diagnosis

>2 attacks (relapses) with >2
objective Clinical lesion
>2 attacks with 1 objective clinical
lesion
None
 MRI: spatially disseminated lesions or
 +ve CSF and >2 MRI lesion
 2nd attack at a new site

1 attack with >2 objective clinical  Dissemination in time.

lesion  New lesion on repeat MRI after >3 months
 2nd attack

1 attack with 1 objective clinical  Dissemination in space

lesion (monosymptomatic  MRI or +ve CSF if >2 MRI lesions consistent with MS
presentation)  And Dissemination in time (by MRI or 2nd clinical attack)

Insidious neurological progression  +ve CSF and dissemination in space on MRI/VEP or

suggestive of primary progressive Continued progression for >1 yr
MS

Careful history may revel past episodes e.g. brief unexplained visual loss and detailed examination may
show more than 1 lesion

Attacks must last >1h with >30d between attacks.

Step wise Management NICE 2014 CG186

1. For acute exacerbation (new symptoms or worsening of
existing symptoms lasting more than 24 hours in the
absence of infection or other causes.
- Offer oral Prednisolone or IV methylprednisolone
2. Prevent relapse using disease- modifying therapies
- Interferon-beta SC reduces relapse by 30-40%
- Glatiramer acetate SC an immunomodulating drug
reduces relapse by 30%
- Dimethyl fumarate, teriflunomide, alemtuzumab is the
option for mild/moderate Relapsing remitting MS
Symptomatic management of MS
Fatigue – Amantadine, CBT, Supervised exercise
Balance- vestibular rehabilitation
Spasticity- Baclofen or gabapentin as first line treatment
Neuropathic pain – Amitriptyline, duloxetine, pregabalin or gabapentin
Bladder incontinence – may attempt intermittent self-catherization or
anticholinergics
Six MS Eponyms
1. Devic’s syndrome: (=neuromyelitis optica,
NMO) MS variant with transverse myelitis(
loss of motor, sensory, autonomic, Reflex
and sphinicter function below the level of a
lesion) optic atrophy and antiaquaporin 4
antibodies
2. Lhermitte Sign: Neck Flexion causes ‘elctric
shocks’ in trunks/ limbs.(Also +ve in cervical
spondylosis, cord tumours and low B12)
3. Uhthoff’s phenomenon: worsening
symptoms with heat e.g in a bath
4. Charles Bonnet syndrome: Decrease
acuity/temporary blindness +/- complex
visual hallucination of face as well as
animals, plants and trees
5. Pulfrich effect: unequal eye latencies
causing disorientation in traffic as straight
trajectories of faces seemed curved and
distances are misjudged on looking
sideways
6. Argyll Robertson pupil
Haemorrhage
Subarachnoid haemorrhage

 Bleeding into the Pia mater and subarachnoid

space
Symptoms and Signs
 Sudden onset excruciating headache typically
occipital “like a thunder clap”
 Vomiting
 Collapse
 Seizures and coma

Signs  Neck stiffness (Kernig’s sign) retinal,

subhyaloid bleed (=Terson’s syndrome). Focal
neurology at presentation may suggest site of aneurysm. (pupil changes indicating a third nerve palsy with a PCAA)

Causes
 Traumatic head injury
 Rupture of a Saccular “Berry” aneurysm (Berry aneurysm are associated with Polycystic kidney disease and
connective tissue disorders such as Marfan and coarctation of the aorta)
 Space occupying lesions, vasculitis, encephalitis, tumour
 Arterio-venous malformations (the is abnormal malformation)

Risk Factors
o Previous Hx of SAH,
o Smoking and alcohol misuse
o Increased BP
o Family history of SAH
o Connective tissue disease – Marfans, Ehlers-Danlos
o PKD, Coarctation of the aorta
Investigation
1. Arrange CT
First choice – detects 95% of SAH within the 1st 24 hours
2. Consider a LP
If SAH is suspected and the CT is negative
Perform after 12 h allowing sufficient time for red cell lysis to occur
Management
 Immediate referral to neurosurgery
 Re-examine the CNS often; chart Blood pressure, pupils and GCS- Repeat CT
 Maintain cerebral perfusion by keeping well hydrated but am for SBP <160mmhg
 Nimodipine (60mg/4hPO for 3 weeks or 1mg/h IVI) reducing vasospasm and consequent morbidity from
cerebral ischemia
 Surgery: Endovascular coiling

Complications
1. Rebleeding – common cause of death
2. Cerebral ischemia – due to vasospasm may cause permanent CNS deficit
3. Hydrocephalus – due to blockage of the arachnoid granulation requires a ventricular or lumbar drain

Subdural Haematoma

A subdural haematoma refers to the pooling of blood in

the subdural space.
The bleeding is from bridging veins between the cortex
and venous sinuses resulting in accumulating haematoma
between the dura and arachnoid.

 This gradually raises the ICP, shifting midline

structures away from the side of the clot and if
untreated eventually tentorial herniation and coning

 Subdural haematoma may be associated with

vigorous coup and counter coup forces – Shaken baby
syndrome

Older individual or alcoholic are also likely to develop

subdural haematoma as a result of cerebral atrophy

Signs and symptoms

 Seizure
 Localizing neurological symptoms (unequal pupils
which may occur late)
 Fluctuating level of consciousness + insidious physical and intellectual slowing, sleepiness,
headache, personality change and unsteadiness, incontinence
Investigation
1. CT/MRI showing clot plus midline shift.
2. Look for crescent shaped collection of blood over the 1 hemisphere The sickle shape
differentiates Subdural from extradural
Management
- Reverse clotting abnormalities.
- Surgical management: depends of size of clot (those that are >10mm or with a midline shift >5mm
need evacuating – craniotomy or burr hole washout)
- Address the trauma – fall or abuse
Extradural haematoma
An extradural haematoma refers to the pooling of blood between the dura mater and the skull.
It is most commonly a result of trauma particularly middle meningeal artery rupture in the context of a
fracture

Patient present with history of trauma accompanied by lucid interval in which the patients GCS
deteriorates over hours to days
Other clinical features:
- The lucid interval last for hours or days declared by decreased GCS and a rising ICP
- Increasingly severe headache
- Vomiting, confusion, seizures
- Hemiparesis with brisk reflexes and upgoing plantar
- If bleeding continues the ipsilateral pupil dilates and the coma deepens, bilateral weakness
develops

Test -CT scan to show haematoma (often biconvex/lens shaped, the blood forms a more rounded shape
compared with the sickle shaped subdural haematoma a the tough dural attachment keep it more
localised

MEDICATIONS
▪Mannitol, other osmotic diuretics
▫↑urine excretion, ↓intracranial pressure
▪Anticoagulation reversal
▫Individuals undergoing surgery, on anticoagulation therapy
SURGERY
▪Craniotomy
▫Evacuation of blood mass
▪Embolization/ligation of damaged blood vessel
▪Trephination (burr-hole)
▫ In acute EDH, if neurosurgical procedure delayed
▪Laminectomy (laminectomy enlarges your spinal canal to relieve
pressure on the spinal cord or nerves)
▫↓ blood in spinal epidural hematoma

Prognosis – Excellent if diagnosis and operation early. Poor if coma, pupil

abnormalities or decerebrate rigidity ARE PRESENT
Vasculitis
 The Vasculitides are inflammatory disorders of blood vessels commonly classified using the
modified Chapel Hill criteria
 They could affect any organ and presentation depends on the organs involved.
 Could be a primary condition or secondary to other diseases – SLE, RA, Hep B&C HIV.
 Categorised by the size of the blood vessels affected
Giant Cell arteritis AKA Temporal arteritis

 Common in the elderly – Consider Takayasu if the patient is less than 55 years
 Associated with PMR
 The risk  irreversible Bilateral vision loss if not treated
Symptoms

Test
- ESR and CRP (should be very high)
- Increased platelets
- Increased ALP
- Decreased Hb
- Temporal artery biopsy with 14 days of starting steroids

Management
 Prednisolone 60 mg PO immediately or
 IV methylprednisolone – if evolving visual loss
Myasthenia Gravis
MG is an autoimmune disease mediated by antibodies to Nicotinic acetylcholine receptors (AChr)on the
post synaptic side of the neuromuscular junction.
Presentation
 Slowly increasing or relapsing muscular fatigue. Muscle groups affected are 
o Extraocular
o Bulbar (swallowing, chewing)
o Face and neck
o Limb girdle and trunk
Signs –
o Ptosis, diplopia
o myasthenic snarl or smiling
o ‘peek sign’ of orbicularis fatigability
(eyelids separate after manual opposition
to sustained closure)
o On counting to 50 – Voice fades
(dysphonia is a rare presentation)
Symptoms are exacerbated by:
 Pregnancy
 Decreased serum Potassium
 Infection, emotion, climate
 Gentamicin, opiated, tetracycline, quinine,
Beta blockers

 Rarely it is caused by a genetic defect in

the neuromuscular junction  Congenital
Myasthenia
 Babies with mother mothers that have MG show symptoms during the first months of life 
Neonatal Myasthenia
Risk factors: FHx of autoimmune disorders, genetic markers
Signs: muscle fatigue, Ptosis, diplopia, Dysphagia
Diagnosis: Serum acetylcholine receptor (AChR) antibody analysis. Muscle-specific kinase (MuSK)
antibodies. Serial pulmonary function test.

Treatment:
- Acutely severe: Intubation/mechanical ventilation + IV immunoglobulin (400mg/Kg). +/- Rituximab
(immunosuppressant). Or Prednisolone (to inhibit immune system 1-1.5mg/kg)
- Mild class I/II: Pyridostigmine 30-60mg (cholinesterase inhibitor- used to improve muscle strength). +/-
Thymectomy
- Moderate class III: Pyridostigmine +/- immunosuppressant + Thymectomy + IV immunoglobulin
Intracranial venous Thrombosis
Thrombosis of cerebral sinuses or veins causes cerebral infraction – though Less common than arterial
disease
Seizure are common and focal – complicate diagnosis and post-ictal drowsiness may impair GCS
assessment

Dural venous sinus thrombosis

Most commonly sagittal sinus thrombosis or Traverse sinus thrombosis.
Sagittal sinus thrombosis often co-exists of other sinus are thrombosed
Symptom onset is gradual features depend on the sinus affected

Sagittal sinus Headache , vomiting , seizures , vision, papilledema

Transverse sinus Papilledema, Headache + mastoid pain, Focal CNS signs , seizures

Sigmoid sinus Cerebellar signs , lower cranial nerve palsies

Inferior petrosal sinus Vth and VIth cranial nerve palsies with temporal and retro orbital pain
Gradinego syndrome suggesting otitis media is the cause

Cavernous sinus Often due to spread from facial pustules or folliculitis causing headache
chemosis(swelling of the conjunctiva), oedematous eyelids, painful
ophthalmoplegia (paralysis of muscles surrounding the eye) , proptosis

Cortical vein thrombosis CVT

 Usually occurs with a sinus thrombus as it extends into the cortical veins causing infraction in a
venous territory
 Infracts give rise to stroke like focal symptoms – often seizures and associated headaches which
may come on suddenly (thunderclap)

- Pregnancy , combined OCP , head injury, dehydration , recent LP, tumours

- Infection (meningitis, otitis media, cerebral malaria , TB)
- Drugs antifibrinolytics androgens ,
- SLE , vasculitis, Crohns , UC

- Exclude subarachnoid haemorrhage and meningitis ,

- Thrombophilia screening
- CT/MRI
- LP – CSF will be normal but may show RBCs and Xanthrochromia
–
- anticoag with heparin or LMWH- and warfarin
- decompressive hemicraniectomy may prevent impending herniation
Peripheral nerve lesions (wrist/foot drop)

Wrist drop
 A condition in which the wrist and fingers cannot extend at the meta-carpophalangeal joints
 The wrist is partially flexed due to the flexor muscles of the forearm & the posterior compartments
remain paralysed
Causes: stab wounds to the chest/below the clavicle (damage to the brachial plexus) so the person develops
neurological deficits inc. inability to abduct should be beyond 15 degrees and extend the forearm. Broken
humerus- damage to radial nerve and maybe the deep brachial artery. Lead poisoning (affects the radial
artery). Persistent injury. Neuropathy.

Diagnosis: nerve conduction velocity (studies nerve conduction; speed). Inability to extend the thumb into
a hitch-hiker’s sign. X-ray to identify bone spurs

Treatment: splinting, physiotherapy, occupational therapy, remove the bony spurs

Foot drop

Is a gait abnormality in which the forefoot happens due to weakness, irritation or damage to the common
fibular nerve (including sciatic nerve) or paralysis of the muscle in the anterior part of the foot?
Drop foot is usually a symptom of a problem and not a disease by itself
 It can be temporary or permanent depending on how weak the muscles are or the degree of
paralysis
 The person can’t raise their toes or the foot from below the ankle (dorsiflexion). When they walk
they limp to prevent dragging the foot sometimes they drag
Cause: damage to a muscle or spinal cord, abnormal anatomy, toxins or disease. Toxins
(organophosphates- pesticides) Diseases (stroke, muscular dystrophy, MS, Gullian Barre syndrome), spinal
stenosis, disc herniation

Treatment: treat the underlying condition. Functional Electrical stimulation is a technique where
electrical are used to activate

Sarcoid
A disease in which there is a collection of inflammatory cells that form a lump known as granuloma
The disease usually begins in the lungs, skin, and lymph nodes. Less common in eyes, liver, heart, brain
Any organ can be affected.
Lungs: SOB, wheezing, coughing, chest pain

Cause: unknown, immune reaction to an infection

Diagnosis: biopsy, enlarged lymph nodes at the root of the lungs, hypercalcaemia with normal PTH, high
levels of angiotensin converting enzyme in serum. Exclude TB

Treatment: ibuprofen (to stop inflammation), Prednisone. In severe cases  methotrexate/azathioprine

Neoplasms of the brain/spinal cord
 Two types (malignant and benign)
 Produce symptoms signs of high intracranial pressure: headaches (worse in morning & goes away with
vomiting), seizures, vision problems, vomiting, mental changes, difficulty walking, speaking or with
sensation  in advanced stages syncope
 The tumour can grow anywhere in the tissues within the cranium (brain, cranial nerves, meninges,
skull, pituitary gland, pineal gland)

Meningioma Primary tumour of the cranial & spinal compartments (meninges). More
common in women and benign. They may also produce a visible growth.
Diagnosis: MRI (with/without contrast. Surgically removed, some cases
they get local radiation

Vestibular Benign, slow growing that usually grows from the vestibular component
schwannoma of the vestibulocochlear nerve. Presents with unilateral sensorineural
hearing loss. Causes vertigo, and unilateral facial numbness (facial nerve
is pressed)

Medulloblastoma Malignant, invasive brain tumour that arises from cerebellar vermis.
They arise sporadically by the age of 20yrs (most common in kids). Signs-
diplopia, vomiting, hydrocephalus. CT/MRI Is used and surgery,
radiation, chemo are used.

Astrocytic brain Primary tumour arising from astrocytes which make up the blood-brain
tumours barrier. More common in white men. Diagnosis: cranial imaging, surgical
biopsy (because the tumour causes histological changes). Treatment:
radio, chemo, surgery.

Craniopharyngioma Benign non-glial epithelial tumour of the CNS arises from sellar/subsellar
space. More common in 5-14yrs &50-70yrs.
The kids present with growth failure, adults- diabetes, and sexual
dysfunction. Diagnosis: CT/MRI. Treatment: surgery, radio.
Primary CNS Rare & malignant cells develop in lymph nodes in brain and spinal cord.
lymphoma Risk factors: immunosuppression, HIV, EBV. Diagnosis: cranial CT, clinical
history, Lumbar puncture, CSF. Treatment: methotrexate-base chemo +
cytarabine + whole brain radio.
Acromegaly, Cushing Acromegaly - due to a pituitary somatotroph adenoma secreting
syndrome,
excessive GH, which stimulates insulin-like growth factor-1 (IGF-1)
prolactinoma, pituitary
production, leading to the majority of the clinical manifestations of the
mass
acromegaly
Cushings syndrome - hypercortisolism caused by an ACTH-secreting
pituitary adenoma
Prolactinoma - Benign prolactin-expressing and secreting pituitary
adenoma
Raised intracranial pressure
 The volume inside the cranium is fixed – so any increase in the contents can lead to raised ICP
 Causes oedema ,obstruction to fluid outflow
 NORMAL ICP in Adults - <15mmHg

 Space occupying lesions

 Infections – meningitis ,encephalitis , brain abscess
 Hydrocephalus - U&E, FBC, LFT, Glucose ,
 Cerebral oedema Serum osmolality, clotting ,
 Status epilepticus Blood culture
 Haemorrhage – subdural, extradural, subarachnoid, - Consider toxicology
intracerebral, intraventricular screening
- CT head
 Headache –( worse when coughing and leaning forward ), - LP if safe – measure
vomiting opening pressure
 Altered GCS drowsiness, irritability
 Visual problems
o Ptosis
o Cranial nerve (iii and Vi ) palsies
o Blurring of optic disc, hyperaemia and papilledema
Hydrocephalus
An increase in the circulating volume of CSF with the cerebral ventricles

Classed into 4 forms

- Communicating
o Impaired absorption of CSF
o No obstruction to CSF flow within the ventricles
o Causes include subarachnoid haemorrhage, meningitis
- Non communicating (obstructive)
o May be due to congenital abnormalities or acquired (bleeding, infection, tumours)
- Normal pressure hydrocephalus
o Normal to mildly elevated pressure
o Triad of urinary elevated pressure
o Triad of urinary incontinence, dementia , and gait disturbances
o Wet , wacky and wobbly
o Gait id described as magnetic
- Hydrocephalus ex vacuo
o Compensatory dilation of ventricles and spaces in response to brain atrophy (dementia)

1. Elevate head (to improve drainage ) and provide oxygen and ventilation
 Target PO2 >13 kPa
 Target pCO2 : 4.5kPa
2. Treat pyrexia (if present )
3. Prescribe Mannitol or hypertonic saline
 Give 20% solution 0.25- 0.5g/kg IV over 10-20 min
 Causes osmotic diuresis and initial reduction of CSF
 May later cause a rebound increase in ICP
 Give as bolus as opposed to continuous infusion