Neurology

Question 1

What are the main 2 classifications of seizures? How are they further classified?

Answer 1

Focal
::::: 1. Focal aware
::::: 2. Focal impaired awareness
::::: 3. Focal to bilateral tonic-clonic seizures - begins in one hemisphere then involves both hemispheres
=================
Generalised
::::: 1. tonic-clonic - tonic phase (stiff) then clonic phase (jerking)
::::: 2. absence
::::: 3. myoclonic - brief jerks/twitches of muscles or muscle groups
::::: 4. tonic - sudden increased tone in extensor muscles
::::: 5. atonic - drop attacks
::::: 6. clonic - rhythmic jerking without initial tonic phase

Question 2

What are first line investigations for epilepsy?

Answer 2

EEG - normal does not exclude, abnormal dose not confirm
:::::
MRI - to identify abnormalities that may cause seizures e.g masses, VM’s, cortical dysplasias

Question 3

What are further investigations for epilepsy?

Answer 3

Video-EEG monitoring - over several days
:::::
PET/SPECT scan (positron emission tomogrophy/single-photon emission computed tomography) - functional brain imaging, can localise seizure focus

Question 4

What is the 1st line anti-epileptic in adults with newly diagnosed focal or gen ton-clonic seizures?

Answer 4

Carbamazepine or lamotrigine

Question 5

What is the 1st line anti-epileptic in children/young ppl with generalised seizures?

Answer 5

Levetiracetam (Keppra) or valproate

Question 6

What is the 1st line anti-epileptic in children/young ppl with focal seizures?

Answer 6

Carbamazepine or lamotrigine

Question 7

What is the next step if seizures are not controlled with a single anti-epileptic drug? What is the next step after?

Answer 7

Second AED introduced e.g. sodium valproate (C/I: childbearing), lamotrigine, levetiracetam and topiramate
………….
if dual AED ineffective, refer to tertiary epilepsy specialist, ketogenic diet, vagus nerve stimulation
………
Surgical: resective surgery (e.g., temporal lobectomy), disconnection procedures (e.g., corpus callosotomy) and neuromodulation techniques (e.g., deep brain stimulation).

Question 8

MoA and S/E of sodium valproate

Answer 8

increases activity of GABA (gamma-aminobutyric acid)

S/E:
- Teratogenic (harmful in pregnancy) - neural tube defects, developmental delay
- Liver damage and hepatitis
- Hair loss
- Tremor
- Reduce fertility

Question 9

Management of status epilepticus

Answer 9

1. ABCDE
2. benzo after 5 mins:
   - buccal midazolam 10mg
   - PR diazepam 10mg
   - IV lorazepam 4mg
3. rpt after 5 mins
4. IV keppra, phenytoin or sodium valproate
5. phenobarbiital or general anaesthesia

Question 10

Protective factors for Parkinson’s Disease

Answer 10

Smoking
Caffeine
Physical activity

Question 11

Risk factors for PD

Answer 11

FHx
Prev head injury

Question 12

Pathophysiology of PD

Answer 12

neurodegenerative disorder characterised by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc), leading to dopamine deficiency in the striatum

cell death in SNpc
increased oxidative stress
misfolding and aggregation of proteins
accumulation of Lewy bodies (misfolded α-synuclein)
synaptic dysfunction
neuronal death
neuroinflammation

Question 13

3 major clinical features of PD. other motor features

Answer 13

resting tremor
+
muscle rigidity
+
bradykinesia
===============
pill rolling tremor :: unilateral then bilateral :: intermittent tremor
cogwheel rigidity :: stooped posture :: reduced arm swing ::
progressive reduction in amplitude of repetitive movements :: shuffling gait :: dragging feet
postural instability
mask-like face (hypomimia) :: micrographia :: dysphagia

Question 14

non-motor symptoms of PD

Answer 14

mood disturbance: depression, apathy, anxiety
…………
psychiatric symptoms: psychotic eps, visual
hallucinations, paranoid delusions, dementia
………….
sleep dysfunction: RLS, insomnia

Question 15

How is PD diagnosed? Diagnostic and exclusion criteria

Answer 15

clinical diagnosis

inv only if uncertainty but not recommended :
- structural MRI
- SPECT

Diagnostic criteria:
bradykinesia + 1 of:
- muscular rigidity
- resting tremor (4-6 Hz freq)
- postural instability

Exclusion criteria (there’s a lot), multiple of:
- History of repeated strokes with stepwise progression of parkinsonian clinical features
- History of repeated head injury
- History of definite encephalitis
- History or current oculogyric crises
- Neuroleptic treatment at time of symptom onset
- More than one affected relative
- Sustained remission
- Strictly unilateral features after 3 years (Note: Parkinson’s progresses from unilateral to the contralateral side with time, but the initial side affected tends to remain more greatly impacted)
- Supranuclear gaze palsy
- Cerebellar signs
- Early severe autonomic involvement (Note: consider multiple system atrophy)
- Early severe dementia with disturbances of memory, language, and praxis
- Positive babinski sign
- Presence of cerebral tumour or communication hydrocephalus on imaging
- Negative response to large doses of levodopa in absence of malabsorption
- MPTP exposure (a compound which causes selective degeneration of the substantia nigra, in users of illicit drug MPPP contaminated with MPTP)

Question 16

Medications for PD. Alternatives?

Answer 16

Levodopa with carbidopa and entacapone
- good for >65 y/o

MAO-B (monoamine oxidase B) inhibitors (if not impacting QoL)

Dopamine agonists e.g. ropinrole (if not impacting QoL)

Alternatives: deep brain sitmulation

Question 17

Complications of PD:

Answer 17

autonomic dysfunction
recurrent falls
cognitive impairment - dementia

Question 18

Name three bacterial causes of meningitis.

Answer 18

Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae.

Question 19

What is the distinguishing feature of meningococcal septicaemia?

Answer 19

A non-blanching rash.

Question 20

Which viruses commonly cause viral meningitis?

Answer 20

Enteroviruses, herpes simplex virus (HSV), and varicella zoster virus (VZV).

Question 21

What is a positive Kernig’s test in meningitis?

Answer 21

Pain or resistance when extending the knee while the hip is flexed at 90 degrees.

Question 22

What is a positive Brudzinski’s test in meningitis?

Answer 22

Involuntary flexion of the hips and knees when the patient’s neck is flexed.

Question 23

In a lumbar puncture, what cerebrospinal fluid (CSF) findings indicate bacterial meningitis?

Answer 23

Cloudy appearance, high protein, low glucose, and high white cell count (mainly neutrophils).

Question 24

What antibiotic is typically used for children over 3 months with bacterial meningitis?

Answer 24

Ceftriaxone

Question 25

Why are steroids like dexamethasone used in bacterial meningitis?

Answer 25

To reduce the frequency and severity of hearing loss and neurological complications.

Question 26

What is the recommended post-exposure prophylaxis for significant contact with meningococcal meningitis?

Answer 26

A single dose of ciprofloxacin.

Question 27

When performing a lumbar puncture, where is the needle typically inserted?

Answer 27

L3-L4 or L4-L5 intervertebral space.

Question 28

What is the most common viral cause of encephalitis in children?

Answer 28

Herpes simplex virus type 1 (HSV-1), commonly associated with cold sores.

Question 29

Which virus is the main cause of encephalitis in neonates, and how is it transmitted?

Answer 29

Herpes simplex virus type 2 (HSV-2), contracted during birth from genital herpes.

Question 30

Name four other viral causes of encephalitis besides herpes simplex virus.

Answer 30

Varicella zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr virus (EBV), and enterovirus.

Question 31

What are the key symptoms of encephalitis?

Answer 31

Altered consciousness, cognition, unusual behavior, focal neurological symptoms, focal seizures, and fever.

Question 32

What diagnostic tests are essential for encephalitis?

Answer 32

Lumbar puncture for viral PCR, CT or MRI scans, and EEG if necessary.

Question 33

When is a lumbar puncture contraindicated in encephalitis?

Answer 33

When the patient has a GCS below 9, is haemodynamically unstable, has active seizures, or is in a post-ictal state.

Question 34

What are the main complications of encephalitis?

Answer 34

Lasting fatigue, personality changes, memory issues, learning disability, seizures, headaches, and movement disorders.

Question 35

What is the role of ganciclovir in treating encephalitis?

Answer 35

It is used to treat cytomegalovirus (CMV) encephalitis.

Question 36

What are the five branches of the facial nerve after it passes through the temporal bone and parotid gland?

Answer 36

Temporal, Zygomatic, Buccal, Marginal Mandibular, Cervical.

Question 37

What is the motor function of the facial nerve?

Answer 37

Controls facial expression, stapedius in the ear, and the posterior digastric, stylohyoid, and platysma muscles.

Question 38

What sensory function does the facial nerve provide?

Answer 38

Taste sensation from the anterior two-thirds of the tongue.

Question 39

Which parasympathetic functions are controlled by the facial nerve?

Answer 39

Stimulation of tear production (lacrimal gland) and saliva production (submandibular and sublingual salivary glands).

Question 40

How can you distinguish between upper and lower motor neurone facial nerve palsy?

Answer 40

In an upper motor neurone lesion, the forehead is spared (patient can move the forehead). In a lower motor neurone lesion, the forehead is not spared (patient cannot move the forehead).

Question 41

What is the recommended treatment for Bell’s palsy if symptoms present within 72 hours?

Answer 41

Prednisolone: either 50mg for 10 days or 60mg for 5 days followed by a tapering dose for another 5 days.

Question 42

What is Ramsay-Hunt syndrome, and how is it treated?

Answer 42

It is a lower motor neurone facial nerve palsy caused by varicella zoster virus, often with a painful vesicular rash around the ear. Treated with aciclovir and prednisolone, plus lubricating eye drops.

Question 43

Name three infections that can cause lower motor neurone facial nerve palsy.

Answer 43

Otitis media, HIV, Lyme disease.

Question 44

What types of tumours can cause lower motor neurone facial nerve palsy?

Answer 44

Acoustic neuroma, parotid tumour, cholesteatoma.

Question 45

What is a major complication of untreated Giant Cell Arteritis?

Answer 45

Vision loss, which is often irreversible.

Question 46

What is the typical presentation of Giant Cell Arteritis?

Answer 46

Unilateral severe headache, often around the temple and forehead.

Question 47

What are some associated symptoms of Giant Cell Arteritis?

Answer 47

Scalp tenderness, jaw claudication, blurred or double vision, and potentially vision loss if untreated.

Question 48

How can the temporal artery appear in Giant Cell Arteritis?

Answer 48

Tender, thickened, with reduced or absent pulsation.

Question 49

What are the associated features of Giant Cell Arteritis?

Answer 49

PMR,
systemic symptoms (weight loss, fatigue, low-grade fever), muscle tenderness,
carpal tunnel syndrome, and
peripheral oedema.

Question 50

What are the key diagnostic tools for Giant Cell Arteritis?

Answer 50

Clinical presentation, raised ESR (over 50 mm/hour), temporal artery biopsy, and duplex ultrasound showing the “halo” sign.

Question 51

How is Giant Cell Arteritis treated initially without visual symptoms?

Answer 51

With 40-60mg of prednisolone daily until remission

Question 52

What is the initial treatment for Giant Cell Arteritis with visual symptoms or jaw claudication?

Answer 52

500-1000mg of methylprednisolone daily.

Question 53

Which parts of the body are primarily affected by polymyalgia rheumatica (PMR)?

Answer 53

The shoulders, pelvic girdle, and neck, with pain sometimes radiating to the upper arm, elbow, or thighs.

Question 54

What are the characteristic features of pain and stiffness in PMR?

Answer 54

Worse in the morning, worse after rest, interferes with sleep, and takes at least 45 minutes to ease in the morning.

Question 55

What are some associated symptoms of PMR?

Answer 55

Systemic symptoms like weight loss, fatigue, low-grade fever, muscle tenderness, carpal tunnel syndrome, and peripheral oedema.

Question 56

How is polymyalgia rheumatica diagnosed?

Answer 56

Based on clinical presentation, response to steroids, raised inflammatory markers (ESR, CRP), and excluding differential diagnoses.

Question 57

What investigations are recommended before starting steroids in suspected PMR?

Answer 57

Full blood count, renal profile, liver function tests, calcium, serum protein electrophoresis, thyroid function tests, creatine kinase, rheumatoid factor, and urine dipstick.

Question 58

What is the initial treatment for polymyalgia rheumatica?

Answer 58

15mg of prednisolone daily with follow-up after 1 week

Question 59

How quickly should patients with PMR respond to steroids?

Answer 59

There should be at least a 70% improvement in symptoms within one week and normalization of inflammatory markers within one month.

Question 60

What is the typical duration of steroid treatment for PMR?

Answer 60

1-2 years, with a gradual reduction in dose as symptoms and inflammation improve.

Start with 15mg pred daily, then reduce to 12.5mg for 3 weeks, followed by 10mg for 4-6 weeks, and continue reducing by 1mg every 4-8 weeks.