Neurology r/v

Question 1

Answer 1

Answer: Assessment of airway breathing and circulation + fluid resuscitation → do first

(other stuff on the answers will have a place in the management first but first is ABC assessment)

Question 2

Common organisms causing meningitis in adults

Answer 2

• Nisseria Meningitidis
• Haemophilus Influenza B
• Streptococcus Pneumoniae

Question 3

Classic triad of meningitis

Answer 3

• headache
• neck stiffness
• fever

Question 4

Management of meningitis

Answer 4

• IM benzylpenicillin in pre-hospital setting (+ transfer to hospital)
• Antibiotics: ceftriaxone + (in pt >60) add ampicillin/amoxicillin to cover for Listeria

*chloramphenicol if Hx of hypersensitivity reaction to penicillins/ cephalosporins

• IV dexamethasone to reduce the risk of neurological sequelae e.g. deafness

Question 5

Management of contacts in meningitis

Answer 5

• prophylactic antibiotics if they have close contact within the 7 days before the onset
• oral ciprofloxacin or rifampicin
• the risk is highest in the first 7 days but persists for at least 4 weeks
• meningococcal vaccination should be offered to close contacts when serotype results are available, including booster doses to those who had the vaccine in infancy
• for pneumococcal meningitis, no prophylaxis is generally needed. There are however exceptions to this. If a cluster of cases of pneumococcal meningitis occur the HPA have a protocol for offering close contacts antibiotic prophylaxis.

Question 6

Ix in suspected meningitis

Answer 6

• full blood count
• CRP
• coagulation screen
• blood culture
• whole-blood PCR
• blood glucose
• blood gas

Lumbar puncture if no signs of raised intracranial pressure

Question 7

When pt needs CT scan before LP?

Answer 7

If anything suggesting increased intracranial pressure:

• seizures
• reduced GCS
• focal neurological signs

Question 8

Answer 8

First Mx step → IV aciclovir

Clinical suspicion of encephalitis (give treatment before CT scan)

• Pt would require CT head before LP (as lower GCS, seizure)
• so far it was one-off terminating seizure so no anti-epileptic required at this stage

Question 9

Features of encephalitis

Answer 9

• fever, headache, psychiatric symptoms, seizures, vomiting
• focal features e.g. aphasia

Question 10

Pathophysiology of encephalitis

Answer 10

• HSV-1 responsible for 95% of cases in adults
• typically affects temporal and inferior frontal lobes

Question 11

Ix in suspected encephalitis

Answer 11

• CSF: lymphocytosis, elevated protein
• PCR for HSV
• CT: medial temporal and inferior frontal changes (e.g. petechial haemorrhages) - normal in one-third of patients
• MRI is better
• EEG pattern: lateralised periodic discharges at 2 Hz

Management

• intravenous aciclovir should be started in all cases of suspected encephalitis

Question 12

Prognosis in viral encephelitis

Answer 12

The prognosis is dependent on whether aciclovir is commenced early. If treatment is started promptly the mortality is 10-20%. Left untreated the mortality approaches 80%

Question 13

Classical changes on MRI brain in viral encephalitis

Answer 13

white matter changes in temporal region bilaterally

Question 14

Answer 14

Suspected: SAH

Do CT head first

Question 15

Management of SAH

Answer 15

• The treatment in spontaneous SAH is in accordance with the causative pathology
• Intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours
• Most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon
• Until the aneurysm is treated, the patient should be kept on strict bed rest, well-controlled blood pressure and should avoid straining in order to prevent a re-bleed of the aneurysm
• Vasospasm is prevented using a 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature) and treated with hypervolaemia, induced-hypertension and haemodilutiond with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculo-peritoneal shunt

Question 16

Diagnosis?

Answer 16

Idiopathic intracranial hypertension

Question 17

Risk factors for idiopathic intracranial hypertension

Answer 17

Risk factors

• obesity
• female sex
• pregnancy
• drugs: oral contraceptive pill, steroids, tetracycline, vitamin A, lithium

Question 18

Features of idiopathic intracranial hypertension

Answer 18

• headache
• blurred vision
• papilloedema (usually present)
• enlarged blind spot
• sixth nerve palsy may be present

Question 19

Management of idiopathic intracranial hypertension

Answer 19

• weight loss
• diuretics e.g. acetazolamide
• topiramate → the added benefit of causing weight loss in most patients
• repeated LPs
• surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure

Question 20

Diagnosis?

Answer 20

Cluster headache

Question 21

Diagnosis?

Answer 21

Guillain-barre syndrome

Clue: acute neuropathy preceded by diarrhoeal illness

Question 22

Pathophysiology of Guillain - Barre syndrome

Answer 22

Guillain-Barre syndrome describes an immune mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni)

Pathogenesis

• cross reaction of antibodies with gangliosides in the peripheral nervous system
• correlation between anti-ganglioside antibody (e.g. anti-GM1) and clinical features has been demonstrated
• anti-GM1 antibodies in 25% of patients

Question 23

What’s Miller-Fisher syndrome?

Answer 23

Miller Fisher syndrome

• variant of Guillain-Barre syndrome
• associated with ophthalmoplegia, areflexia and ataxia. The eye muscles are typically affected first
• usually presents as a descending paralysis rather than ascending as seen in other forms of Guillain-Barre syndrome
• anti-GQ1b antibodies are present in 90% of cases

Question 24

Buzz- words for Guillain-Barre syndrome

Answer 24

• ascending weakness
• ascending numbness
• areflexia

Question 25

Ix for Guillian-Barre

Answer 25

LP → high protein

Question 26

Where is the lesion?

Answer 26

Common Peroneal nerve The sciatic nerve divides into the tibial and common peroneal nerves. Injury often occurs at the neck of the fibula The most characteristic feature of a common peroneal nerve lesion is foot drop. Other features include: * weakness of foot dorsiflexion * weakness of foot eversion * weakness of extensor hallucis longus * sensory loss over the dorsum of the foot and the lower lateral part of the leg * wasting of the anterior tibial and peroneal muscles

Question 27

The differential diagnosis for unilateral foot drop

Answer 27

Question 28

Diagnosis?

Answer 28

***Transverse myelitis*** infract - happens acutely so not in here acute degeneration - sparing of pinprick as affects dorsal column

Question 29

Ix and Mx of transverse myelitis

Answer 29

* urgent MRI → to exclude compression to spinal cord * LP → possible oligoclonal bands (if disease disseminated in time and space ?MS) Mx: ***IV methylprednisolone***

Question 30

Most likely diagnosis?

Answer 30

Autoimmune myasthenia gravis \*the only drug that induces Myasthenia gravis is penicillamine

Question 31

What's Myasthenia Gravis?

Answer 31

Myasthenia gravis * an autoimmune disorder * insufficient functioning **acetylcholine receptors** * Antibodies to acetylcholine receptors are seen in 85-90% of cases

Question 32

Key features of Myasthenia Gravis

Answer 32

The key feature is muscle fatigability - muscles become progressively weaker during periods of activity and slowly improve after periods of rest: * extraocular muscle weakness: diplopia * proximal muscle weakness: face, neck, limb-girdle * ptosis * dysphagia

Question 33

Associations with Myasthenia Gravis

Answer 33

* thymomas in 15% * autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE * thymic hyperplasia in 50-70%

Question 34

Ix of Myasthenia Gravis

Answer 34

* **single fibre electromyography**: high sensitivity (92-100%) * CT thorax to exclude thymoma * CK normal * autoantibodies: around 85-90% of patients have antibodies to acetylcholine receptors. In the remaining patients, about about 40% are positive for anti-muscle-specific tyrosine kinase antibodies * **Tensilon test**

Question 35

What's tensilon test?

Answer 35

**Tensilon test** (in myasthenia gravis): IV edrophonium reduces muscle weakness temporarily - not commonly used anymore due to the risk of cardiac arrhythmia

Question 36

Management of ***Myasthenia Gravis***

Answer 36

Management * long-acting anticholinesterase inhibitors e.g. ***pyridostigmine*** * **immunosuppression**: prednisolone initially * thymectomy Management of myasthenic crisis * plasmapheresis * intravenous immunoglobulins

Question 37

Diagnosis?

Answer 37

***Dermatomyositis*** Clues for diagnosis: * no muscle wasting, no fasciculation → not a neuropathy or anterior horn cell problems * rash → heliotropic and gottren's papule

Question 38

Management of dermatomyositis

Answer 38

* Monitor regularly → as dermatomyositis may proceed cancer by 5 years (breast, lungs, lymphoma) * Anti-inflammatory * Steroids or steroid-sparing (Methotrexate, azathioprine)

Question 39

Buzzwords for inclusion body myositis

Answer 39

Weakness in: * hip flexors * shoulder girdle * finger flexor * don't respond well to meds

Question 40

Causes of collapse and features

Answer 40

Question 41

Diagnosis?

Answer 41

***Alzheimer's disease*** → as a deficit of working/short-term memory \*vascular dementia would present with the step-like manner \* normal ageing → a person would be worried about their problem (they have insight)

Question 42

Diagnosis?

Answer 42

***Progressive Supranuclear Palsy*** * vertical eye movement -\> PSP * look surprised, overactive frontalis -\> PSP * also: early falls, early wheelchair