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Neurology Flashcards

your lipstick stains, on the front lobe of my left side brain

1
Q

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

A

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

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2
Q

What are first line investigations for epilepsy?

A

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

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3
Q

What are further investigations for epilepsy?

A

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

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4
Q

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

A

Carbamazepine or lamotrigine

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5
Q

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

A

Levetiracetam (Keppra) or valproate

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6
Q

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

A

Carbamazepine or lamotrigine

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7
Q

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

A

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).

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8
Q

MoA and S/E of sodium valproate

A

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

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9
Q

Management of status epilepticus

A
  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
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10
Q

Protective factors for Parkinson’s Disease

A

Smoking
Caffeine
Physical activity

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11
Q

Risk factors for PD

A

FHx
Prev head injury

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12
Q

Pathophysiology of PD

A

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

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13
Q

3 major clinical features of PD. other motor features

A

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

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14
Q

non-motor symptoms of PD

A

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

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15
Q

How is PD diagnosed? Diagnostic and exclusion criteria

A

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)

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16
Q

Medications for PD. Alternatives?

A

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

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17
Q

Complications of PD:

A

autonomic dysfunction
recurrent falls
cognitive impairment - dementia

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18
Q

Name three bacterial causes of meningitis.

A

Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae.

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19
Q

What is the distinguishing feature of meningococcal septicaemia?

A

A non-blanching rash.

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20
Q

Which viruses commonly cause viral meningitis?

A

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

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21
Q

What is a positive Kernig’s test in meningitis?

A

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

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22
Q

What is a positive Brudzinski’s test in meningitis?

A

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

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23
Q

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

A

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

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24
Q

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

A

Ceftriaxone

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25
Q

Why are steroids like dexamethasone used in bacterial meningitis?

A

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

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26
Q

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

A

A single dose of ciprofloxacin.

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27
Q

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

A

L3-L4 or L4-L5 intervertebral space.

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28
Q

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

A

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

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29
Q

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

A

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

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30
Q

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

A

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

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31
Q

What are the key symptoms of encephalitis?

A

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

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32
Q

What diagnostic tests are essential for encephalitis?

A

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

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33
Q

When is a lumbar puncture contraindicated in encephalitis?

A

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

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34
Q

What are the main complications of encephalitis?

A

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

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35
Q

What is the role of ganciclovir in treating encephalitis?

A

It is used to treat cytomegalovirus (CMV) encephalitis.

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36
Q

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

A

Temporal, Zygomatic, Buccal, Marginal Mandibular, Cervical.

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37
Q

What is the motor function of the facial nerve?

A

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

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38
Q

What sensory function does the facial nerve provide?

A

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

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39
Q

Which parasympathetic functions are controlled by the facial nerve?

A

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

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40
Q

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

A

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).

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41
Q

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

A

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

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42
Q

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

A

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.

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43
Q

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

A

Otitis media, HIV, Lyme disease.

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44
Q

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

A

Acoustic neuroma, parotid tumour, cholesteatoma.

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45
Q

What is a major complication of untreated Giant Cell Arteritis?

A

Vision loss, which is often irreversible.

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46
Q

What is the typical presentation of Giant Cell Arteritis?

A

Unilateral severe headache, often around the temple and forehead.

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47
Q

What are some associated symptoms of Giant Cell Arteritis?

A

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

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48
Q

How can the temporal artery appear in Giant Cell Arteritis?

A

Tender, thickened, with reduced or absent pulsation.

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49
Q

What are the associated features of Giant Cell Arteritis?

A

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

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50
Q

What are the key diagnostic tools for Giant Cell Arteritis?

A

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

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51
Q

How is Giant Cell Arteritis treated initially without visual symptoms?

A

With 40-60mg of prednisolone daily until remission

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52
Q

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

A

500-1000mg of methylprednisolone daily.

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53
Q

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

A

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

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54
Q

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

A

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

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55
Q

What are some associated symptoms of PMR?

A

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

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56
Q

How is polymyalgia rheumatica diagnosed?

A

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

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57
Q

What investigations are recommended before starting steroids in suspected PMR?

A

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

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58
Q

What is the initial treatment for polymyalgia rheumatica?

A

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

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59
Q

How quickly should patients with PMR respond to steroids?

A

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

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60
Q

What is the typical duration of steroid treatment for PMR?

A

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.

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61
Q

What are the four main types of migraines?

A

The four main types of migraines are:
- Migraine without aura
- Migraine with aura
- Silent migraine (aura without headache)
- Hemiplegic migraine

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62
Q

What are the typical stages of a migraine?

A

The five stages of a migraine are:
- Premonitory (prodromal) stage
- Aura
- Headache stage
- Resolution stage
- Postdromal (recovery) phase

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63
Q

What is the typical duration of a migraine headache?

A

A migraine headache typically lasts between 4 and 72 hours.

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64
Q

What are common symptoms during the headache stage of a migraine?

A
  • Unilateral or bilateral headache
  • Moderate-severe intensity
  • Pounding or throbbing pain
  • Photophobia, phonophobia, and osmophobia
  • Nausea and vomiting
  • Aura (in some cases)
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65
Q

What is a hemiplegic migraine, and why is it concerning?

A

A hemiplegic migraine involves unilateral limb weakness (hemiplegia), sometimes with ataxia or impaired consciousness. It can mimic a stroke or TIA, so a stroke must be excluded.

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66
Q

What are the acute treatment options for a migraine attack?

A
  • NSAIDs (e.g., ibuprofen, naproxen)
  • Paracetamol
  • Triptans (e.g., sumatriptan)
  • Antiemetics (e.g., metoclopramide, prochlorperazine)
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67
Q

How do triptans work in treating migraines?

A

Triptans are 5-HT receptor agonists (targeting 5-HT1B and 5-HT1D) that:

  • Cause cranial vasoconstriction
  • Inhibit pain transmission
  • Reduce the release of inflammatory neuropeptides
68
Q

What are some contraindications for using triptans?

A

Triptans are contraindicated in conditions with risks from vasoconstriction, such as:
- Hypertension
- Coronary artery disease
- Previous stroke, TIA, or myocardial infarction

69
Q

What are the typical prophylactic medications for migraines? (3)

A
  • Propranolol (beta-blocker)
  • Amitriptyline (tricyclic antidepressant)
  • Topiramate (anticonvulsant, requires effective contraception)
70
Q

Which therapies are used for migraine prophylaxis in more complex cases?

A

Specialist:
- Pizotifen
- Candesartan
- Sodium valproate
- Monoclonal antibodies (e.g., erenumab, fremanezumab)

71
Q

How are menstrual migraines typically managed?

A

Prophylactic triptans (e.g., frovatriptan or zolmitriptan) can be taken from two days before until three days after the start of menstruation to manage menstrual migraines.

72
Q

Why are migraines with aura a contraindication for the combined contraceptive pill?

A

Both increase the risk of stroke

73
Q

What are the key red flags associated with a headache that indicate a serious underlying cause?

A
  • Fever, photophobia, or neck stiffness (suggests meningitis, encephalitis, or brain abscess)
  • New neurological symptoms (suggests haemorrhage or tumour)
  • Visual disturbance (suggests giant cell arteritis, glaucoma, or tumours)
  • Sudden-onset occipital headache (suggests subarachnoid haemorrhage)
  • Worse on coughing/straining (suggests raised intracranial pressure)
  • Postural changes (worse on standing, lying, or bending over, suggests raised intracranial pressure)
  • Vomiting (suggests raised intracranial pressure or carbon monoxide poisoning)
  • History of trauma (suggests intracranial haemorrhage)
  • History of cancer (suggests brain metastasis)
  • Pregnancy (suggests pre-eclampsia)
74
Q

What are some causes of secondary headaches?

A
  • Infections (e.g., viral upper respiratory tract infection)
  • Obstructive sleep apnoea
  • Pre-eclampsia
  • Head injury
  • Carbon monoxide poisoning
75
Q

What are hormonal headaches, and when do they typically occur?

A

Hormonal headaches, often called menstrual migraines, are related to low oestrogen and have features similar to migraines. They may occur:
- Two days before and the first three days of menstruation
- In the perimenopausal period
- Early pregnancy (headaches in the second half of pregnancy may indicate pre-eclampsia)

76
Q

What is the first-line treatment for trigeminal neuralgia?

A

Carbamazepine is the first-line treatment for trigeminal neuralgia according to NICE CKS (2022).

77
Q

What are the common features of trigeminal neuralgia?

A

intense unilateral facial pain in the distribution of the trigeminal nerve, often described as shooting, stabbing, or burning pain. It may be triggered by activities like touching, talking, eating, or shaving.

78
Q

Why is fundoscopy important in patients with headaches?

A

Fundoscopy helps check for papilloedema, which suggests raised intracranial pressure (e.g., due to a brain tumour, benign intracranial hypertension, or an intracranial bleed).

79
Q

What are the common symptoms of cervical spondylosis, and how does it relate to headaches?

A

Cervical spondylosis causes neck pain often worsened by movement, and may present with headaches due to the degenerative changes in the cervical spine.

80
Q

What are the typical characteristics of cluster headache attacks?

A

Cluster headache attacks last 15 minutes to 3 hours and may occur 3-4 times a day. The pain is severe and often described as unbearable. Remission periods between clusters can last for years.

81
Q

Who is the typical patient suffering from cluster headaches?

A

A typical patient is a 30-50 year old male smoker. Cluster headaches are more common in men, and potential triggers include alcohol, strong smells, and exercise.

82
Q

What are the unilateral symptoms associated with cluster headaches?

A

The unilateral symptoms associated with cluster headaches include:
- Red, swollen, and watering eye
- Pupil constriction (miosis)
- Eyelid drooping (ptosis)
- Nasal discharge
- Facial sweating

83
Q

What are the acute treatment options for cluster headaches?

A

Acute treatment options include:
- Triptans (e.g., subcutaneous or intranasal sumatriptan)
- High-flow 100% oxygen, which may be kept at home

84
Q

What is the first-line prophylactic treatment for cluster headaches? What are other prophylactic treatment options for cluster headaches?

A

Verapamil, a calcium channel blocker.

Other prophylactic options include:
- Occipital nerve block
- Prednisolone (short course to break the cycle during clusters)
- Lithium

85
Q

What is an extradural haemorrhage?

A

An extradural haemorrhage is bleeding between the skull and dura mater, typically caused by rupture of the middle meningeal artery due to trauma.

86
Q

What is a subdural haemorrhage?

A

A subdural haemorrhage is bleeding between the dura mater and arachnoid mater, often caused by rupture of bridging veins.

87
Q

Which types of intracranial haemorrhage are most commonly associated with strokes?

A

Intracerebral and subarachnoid haemorrhages, accounting for 10-20% of strokes.

88
Q

List some common risk factors for intracranial haemorrhage.

A
  • Head injuries,
  • hypertension,
  • aneurysms,
  • ischemic strokes,
  • brain tumors,
  • thrombocytopenia,
  • bleeding disorders,
  • anticoagulants.
89
Q

What are typical symptoms of an intracranial haemorrhage?

A
  • Sudden-onset headache,
  • seizures,
  • vomiting,
  • reduced consciousness,
  • focal neurological symptoms.
90
Q

What does a Glasgow Coma Scale (GCS) score of 8/15 indicate?

A

A GCS score of 8/15 or lower indicates a need for airway support due to the risk of airway obstruction or aspiration.

91
Q

How is the Glasgow Coma Scale (GCS) scored?

A

GCS is scored based on eye, verbal, and motor responses, with a maximum score of 15 and a minimum of 3.
SEE TABLE

92
Q

What does a bi-convex shape on a CT scan indicate in relation to intracranial haemorrhages?

A

A bi-convex shape on a CT scan suggests an extradural haemorrhage, which is limited by the cranial sutures.

93
Q

What does a crescent shape on a CT scan suggest in the context of intracranial haemorrhage?

A

A crescent shape suggests a subdural haemorrhage, which can cross cranial sutures.

94
Q

What is the typical history for a patient with an extradural haemorrhage?

A

A young patient with head trauma, an initial period of improved symptoms, followed by rapid decline due to haematoma expansion.

95
Q

Why are elderly and alcoholic patients at higher risk for subdural haemorrhages?

A

Due to brain atrophy, which stretches the bridging veins, making them more prone to rupture.

96
Q

What are the main types of intracerebral haemorrhages based on location?

A

Lobar, deep, intraventricular, basal ganglia, and cerebellar haemorrhages.

97
Q

What immediate steps should be taken in the management of intracranial haemorrhage?

A

Immediate imaging (CT head), blood tests (including coagulation screen), and admission to a specialist stroke center.

98
Q

What surgical treatments are available for extradural or subdural haemorrhages?

A

Craniotomy and burr holes.

99
Q

Why is it critical to identify a subarachnoid haemorrhage quickly?

A

Because it has a high mortality rate (around 30%) and significant morbidity.

100
Q

Which age group and demographics are at higher risk for subarachnoid haemorrhage?

A

It is more common in people aged 45-70, women, and those of Black ethnic origin.

101
Q

What general lifestyle factors increase the risk of subarachnoid haemorrhage?

A

smoking, and excessive alcohol intake, cocaine use

102
Q

What specific conditions are associated with an increased risk of subarachnoid haemorrhage?

A

Family history, cocaine use, sickle cell anemia, connective tissue disorders, neurofibromatosis, and autosomal dominant polycystic kidney disease.

103
Q

What is the typical presentation of a subarachnoid haemorrhage?

A

A sudden, severe occipital headache during strenuous activity, described as a “thunderclap headache.”

Neck stiffness, photophobia, vomiting, neurological symptoms (e.g., visual changes, dysphasia, focal weakness, seizures, reduced consciousness).

104
Q

What is the first-line investigation for suspected subarachnoid haemorrhage?

A

CT head scan, which shows hyper-attenuation in the subarachnoid space if bleeding is present.

105
Q

When should a lumbar puncture be performed in suspected subarachnoid haemorrhage?

A

After a normal CT head, at least 12 hours post-symptom onset to allow bilirubin to accumulate in the CSF.

106
Q

What CSF findings indicate subarachnoid haemorrhage?

A

Raised red cell count and xanthochromia (yellow color in CSF caused by bilirubin).

107
Q

Why is CT angiography used following a diagnosis of subarachnoid haemorrhage?

A

To locate the source of the bleeding.

108
Q

Where should patients with subarachnoid haemorrhage be managed?

A

In a specialist neurosurgical unit, with possible intubation and ventilation if consciousness is reduced.

109
Q

What are the two main surgical interventions to treat aneurysms in subarachnoid haemorrhage?

A

Endovascular coiling and neurosurgical clipping.

110
Q

How does endovascular coiling work to treat aneurysms?

A

A catheter is used to place platinum coils in the aneurysm, sealing it off from the artery.

111
Q

Which medication is used to prevent vasospasm following a subarachnoid haemorrhage?

A

Nimodipine, a calcium channel blocker.

112
Q

What is hydrocephalus, and how might it be managed in subarachnoid haemorrhage?

A

Hydrocephalus is the buildup of cerebrospinal fluid in the ventricles; managed with lumbar puncture, external ventricular drain, or a ventriculoperitoneal (VP) shunt.

113
Q

Which age group and gender are more commonly affected by MS?

A

MS typically affects young adults under 50 and is more common in women.

114
Q

What cells provide myelin in the central and peripheral nervous systems?

A

Oligodendrocytes in the CNS and Schwann cells in the PNS.

115
Q

What does “disseminated in time and space” mean in the context of MS?

A

MS lesions vary in location and timing, causing different symptoms over time

116
Q

Name some factors that may influence the development of MS.

A

Genetic factors, Epstein–Barr virus (EBV), low vitamin D, smoking, and obesity.

117
Q

How long do MS symptoms typically last during the first presentation?

A

Symptoms often last days to weeks before improving.

118
Q

What is the most common initial presentation of MS?

A

Optic neuritis, a demyelination of the optic nerve causing unilateral vision loss.

119
Q

List key features of optic neuritis in MS.

A
  • Central scotoma,
  • eye pain with movement,
  • impaired color vision
  • relative afferent pupillary defect.
120
Q

What are other possible causes of optic neuritis besides MS?

A
  • Sarcoidosis,
  • systemic lupus erythematosus,
  • syphilis,
  • measles,
  • mumps,
  • neuromyelitis optica,
  • Lyme disease.
121
Q

What eye movement abnormalities can occur in MS?

A
  • Double vision (diplopia)
  • nystagmus
  • oscillopsia
  • internuclear ophthalmoplegia.
122
Q

Define internuclear ophthalmoplegia and its cause.

A

A lesion in the medial longitudinal fasciculus causes impaired adduction in the ipsilateral eye and nystagmus in the contralateral eye.

123
Q

Name some focal neurological symptoms that may occur with MS

A

Focal weakness (e.g., limb paralysis, facial nerve palsy), incontinence, and Horner syndrome.

124
Q

What are common sensory symptoms in MS?

A

Trigeminal neuralgia, numbness, paraesthesia, and Lhermitte’s sign.

125
Q

What is Lhermitte’s sign, and what does it indicate?

A

An electric shock sensation down the spine when flexing the neck, indicating cervical spinal cord involvement.

126
Q

What is transverse myelitis?

A

Inflammation in the spinal cord causing sensory and motor symptoms depending on lesion location.

127
Q

What is ataxia, and how does it present in MS?

A

Ataxia is a loss of coordination; sensory ataxia causes balance issues (positive Romberg’s test), and cerebellar ataxia affects movement coordination.

128
Q

Describe “clinically isolated syndrome” in MS.

A

The first episode of demyelination and neurological symptoms, which may or may not progress to MS.

129
Q

What is relapsing-remitting MS?

A

A pattern of MS with episodes of symptoms followed by recovery, with varying activity and worsening over time.

130
Q

How is secondary progressive MS different from primary progressive MS?

A

Secondary progressive MS follows relapsing-remitting MS with a steady worsening of symptoms; primary progressive MS worsens from the start without remissions.

131
Q

What is the role of MRI in diagnosing MS?

A

MRI scans show typical MS lesions, helping support the diagnosis.

132
Q

What is detected in the cerebrospinal fluid (CSF) via lumbar puncture in MS?

A

Oligoclonal bands.

133
Q

How are relapses in MS typically treated?

A

With high-dose steroids, either orally or intravenously

-500mg orally daily for 5 days

  • 1g intravenously daily for 3–5 days (where oral treatment has previously failed or where relapses are severe)
134
Q

Name symptomatic treatments for managing fatigue and neuropathic pain in MS.

A

Fatigue: amantadine, modafinil, or SSRIs;

Neuropathic pain: amitriptyline or gabapentin.

135
Q

Which medications help manage spasticity, urge incontinence, and oscillopsia in MS?

A

Spasticity: baclofen or gabapentin;

Urge incontinence: antimuscarinics like solifenacin;

Oscillopsia: gabapentin or memantine.

136
Q

What is motor neurone disease (MND)?

A

MND is a progressive, fatal condition where motor neurons deteriorate, leading to muscle weakness without affecting sensory neurons.

137
Q

Which motor neurone disease is most common, and who is a well-known individual who had it?

A

Amyotrophic lateral sclerosis (ALS) is the most common form, and physicist Stephen Hawking had ALS.

138
Q

Which form of MND primarily affects the muscles of talking and swallowing?

A

Progressive bulbar palsy.

139
Q

Name two other types of motor neurone diseases besides ALS and progressive bulbar palsy.

A

Progressive muscular atrophy and primary lateral sclerosis.

140
Q

What are some potential risk factors for developing motor neurone disease?

A

Family history (5-10% inherited cases), smoking, exposure to heavy metals, and certain pesticides.

141
Q

What is the typical patient profile for motor neurone disease?

A

A late middle-aged man around 60 years old, possibly with a family history of MND, presenting with progressive muscle weakness.

142
Q

How does motor neurone disease typically present initially?

A

Progressive weakness, often first noticed in the upper limbs, along with clumsiness, dropping objects, tripping, and slurred speech.

143
Q

List the signs of lower motor neurone involvement in MND.

A

Muscle wasting, reduced tone, fasciculations (muscle twitches), and reduced reflexes.

144
Q

What are the signs of upper motor neurone involvement in MND?

A

Increased tone or spasticity, brisk reflexes, and an upgoing plantar reflex.

145
Q

How is motor neurone disease diagnosed?

A

Based on clinical presentation and exclusion of other conditions, and it should be diagnosed by a specialist.

146
Q

Which medication can slow the progression of ALS, and by how much?

A

Riluzole can extend survival in ALS by several months.

147
Q

Name two medications that may help manage symptoms of MND.

A

Baclofen for muscle spasticity and benzodiazepines for breathlessness related to anxiety.

148
Q

What are common causes of death in patients with motor neurone disease?

A

Respiratory failure and pneumonia.

149
Q
A
150
Q

What is myasthenia gravis?

A

An autoimmune condition affecting the neuromuscular junction, causing muscle weakness that worsens with activity and improves with rest.

151
Q

At what ages is myasthenia gravis most likely to affect men and women?

A

Women under 40 and men over 60.

152
Q

What is the association between thymomas and myasthenia gravis?

A

10-20% of myasthenia gravis patients have a thymoma, and 30% of patients with a thymoma develop myasthenia gravis.

153
Q

How does the body normally stimulate muscles at the neuromuscular junction?

A

Motor neurons release acetylcholine, which binds to receptors on the muscle cell, causing contraction.

154
Q

What role do acetylcholine receptor (AChR) antibodies play in myasthenia gravis?

A

AChR antibodies block acetylcholine receptors, preventing muscle stimulation and worsening weakness with use.

155
Q

Name two other antibodies besides AChR antibodies that are associated with myasthenia gravis

A

Muscle-specific kinase (MuSK) antibodies and low-density lipoprotein receptor-related protein 4 (LRP4) antibodies.

156
Q

What are common symptoms of myasthenia gravis?

A

Symptoms include muscle weakness that worsens with activity, difficulty climbing stairs, double vision, ptosis, facial weakness, swallowing difficulty, jaw fatigue, and slurred speech.

157
Q

How can you test for fatiguability in patients with myasthenia gravis?

A

By repeated blinking (worsens ptosis), prolonged upward gaze (worsens diplopia), or repeated arm abduction (causes unilateral weakness).

158
Q

Which antibodies are most commonly tested for diagnosing myasthenia gravis?

A

AChR antibodies (found in 85% of cases), MuSK antibodies (less than 10%), and LRP4 antibodies (less than 5%).

159
Q

How does the edrophonium test work in diagnosing myasthenia gravis?

A

Edrophonium blocks cholinesterase, increasing acetylcholine levels at the neuromuscular junction, which temporarily improves muscle weakness in positive cases.

160
Q

What is the first-line treatment for myasthenia gravis symptoms? What are other treatment options for myasthenia gravis?

A

Pyridostigmine, a cholinesterase inhibitor that prolongs acetylcholine action, improving symptoms.

Other: Immunosuppression (e.g., prednisolone or azathioprine), thymectomy, and rituximab for resistant cases.

161
Q

What is a myasthenic crisis, and why is it dangerous?

A

A myasthenic crisis is an acute worsening of symptoms, often due to an infection, leading to respiratory failure due to weakened respiratory muscles.

162
Q

How is myasthenic crisis treated?

A

With intravenous immunoglobulins and plasmapheresis, and possibly ventilatory support if respiratory failure occurs.

163
Q

According to NICE guidelines, what are the first-line medications for treating neuropathic pain?

A

The first-line treatments are amitriptyline, duloxetine, gabapentin, and pregabalin.

164
Q

What should be done if a first-line neuropathic pain medication is ineffective?

A

If the first-line drug doesn’t work, switch to one of the other three options rather than combining drugs.

165
Q

What medication can be used as ‘rescue therapy’ for exacerbations of neuropathic pain?

A

Tramadol can be used as a rescue therapy for neuropathic pain exacerbations.

166
Q

When might topical capsaicin be used for neuropathic pain?

A

Topical capsaicin may be used for localized neuropathic pain, such as post-herpetic neuralgia.

MSRA (18 decks)

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