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Y4 Special senses > Neurology workbook > Flashcards

Neurology workbook Flashcards

1
Q

Symptoms, key anatomy, conditions and high yield investigations for lesions in the cerebral hemispheres

A

Symptoms
- Motor and sensory loss= contralateral weakness and sensory loss due to corticospinal and spinothalamic tract
- Homonymous hemianopia= contralateral visual field loss from optic radiation
- Speech= Broca’s (expressive) in the frontal lobe. Wernicke’s (receptive) in the temporal
- Neglect syndrome- right hemisphere lesions may cause spatial neglect of the left side
- Disinhibition
Temporal= memory issues

Key anatomy
- Precentral gyrus- motor
- Post-central gyrus- sensory
- Optic radiations in the parietal and temporal lobes

Conditions
- MCA- contralateral hemiparesis, aphasia and neglect
- ACA- contralateral leg weakness
- PCA infarct= visual field defects

High yield investigations
- Imaging- CT head (initial for stroke), MRI for detailed lesion
- Bloods- glucose, coagulation profile and lipids
- EEG= seizure evaluation

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2
Q

Symptoms, key anatomy, conditions and high yield investigations for lesions in the cerebellum

A

Symptoms (DANISH)
- Dysdiadochokinesia
- Ataxia
- Nystagmus
- Intention tremor
- Slurred speech
- Hypotonia

Key anatomy
- Cerebellar hemispheres= fine motor control
- Vermis- balance and posture

Example conditions
- Posterior circulation stroke
- Tumors- astrocytoma, medulloblastoma
- Alcohol induced cerebellar degeneration
- Multiple sclerosis

High yield investigations
- Imaging- MRI brain
- Bloods- B12 deficiency, thyroid function tests
- Alcohol history

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3
Q

Symptoms, key anatomy, conditions and high yield investigations for lesions in the brainstem and cranial nerves

A

Symptoms
- Cranial nerve deficits
- Crossed signs (ipsilateral cranial nerve palsy with contralateral sensory/motor deficit due to corticospinal and sensory tract decussation in the medulla
- Locked in syndrome- preserved eye movements
- Altered consciousness- reticular activating system

Example conditions
- Stroke syndromes (Weber’s (midbrain) and wallenberg (medulla)
- Demyelinating diseases- MS with plaques in the brainstem

Investigations
- MRI for small brainstem infarcts

Sudden onset with cranial nerve and limb findings suggest a brainstem stroke

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4
Q

Symptoms, key anatomy, conditions and high yield investigations for lesions in the basal ganglia

A

Symptoms
Parkinsonism (substantia nigra)
- Pill rolling tremor
- Bradykinesia
- Rigidity
- Postural instability

Huntington’s (striatal degeneration)
- Chorea- involuntary, rapid, jerky movements
- Cognitive decline and psychiatric disturbances
- Dystonia= sustained muscle contractions causing abnormal postures

MRI- striatal atrophy in Huntington’s

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5
Q

Symptoms, key anatomy, conditions and high yield investigations for lesions in the spinal cord

A

Symptoms
Complete cord lesion
- Total loss of motor, sensory and autonomic function

Brown sequard
- Ipsilateral weakness and proprioception/vibration loss
- Contralateral pain/temporal loss

Anterior cord
- Loss of pain/temperature and motor function
- Preservation of proprioception/vibration

Posterior cord
- Loss of prioprioception and vibration sense
- Preservation of motor and pain/temperature sensation

Diagnostic clues
- Trauma, tumours or demyelinating diseases in history

Example conditions
- Trauma (spinal fracture)
-Transverse myelitis, multiple sclerosis

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6
Q

Symptoms, key anatomy, conditions and high yield investigations peripheral nerve lesions

A

Symptoms
- Radiculopathy- dermatomal pain, sensory loss and myotomal weakness (sciatica and cervical radiculopathy)
- Plexopathies- brachial plexus, lumbar plexus
- Peripheral neuropathy- glove and stocking sensory loss. Distal weakness, foot drop

Diagnostic clues
- Chronic conditions= diabetes, alcohol
- Nerve conduction studies

Example conditions
- Guillain-Barre syndrome, diabetic neuropathy

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7
Q

Symptoms, key anatomy, conditions and high yield investigations for neuromuscular junction disorders

A

Symptoms
- Fatigable weakness (ptosis, diplopia worsening with use)
- Bulbar symptoms- dysphagia, dysarthria
- Proximal limb weakness

Diagnostic clues
- Antibodies- Anti-ACHr for myasthenia gravis
- Electromyography- decremental response with repetitive stimulation

Example conditions
- Myasthenia gravis, Lambert-Eaton myasthenic syndrome

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8
Q

Symptoms, key anatomy, conditions and high yield investigations for muscle disorders

A

Symptoms
- Proximal muscle weakness
- Muscle wasting
- NO sensory involvement

Diagnostic clues
- Serum creatine kinase (CK)
- Muscle biopsy for dystrophies

Example conditions
- Duchenne muscular dystrophy, polymyositis

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9
Q

Symptoms, key anatomy, conditions and high yield investigations for nerve root lesions

A

Symptoms
- Motor
- Sensory
- Reflex changes
- Radicular pain- sharp, shooting pain along the dermatomal pathway
- Diagnostic clues

Example conditions
- Cervical or lumbar disc herniation
- Spondylosis with foraminal narrowing

Diagnostic clues
- Pain worsens with movement (neck flexion, SLR)
- MRI spine= nerve root compression
- EMG= nerve root involvement

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10
Q

Symptoms, key anatomy, conditions and high yield investigations for plexopathy

A

Symptoms
- Motor and sensory deficits
- Brachial plexus
- Lumbosacral
- Pain- severe burning pain in the limb
- Autonomic changes- colour changes, temperature intolerance

Diagnostic clues
- History of trauma, malignancy or inflammatory conditions
- Imaging- MRI or CT
- Nerve conduction studies and EMG- localise the lesion and differentiate from peripheral neuropathy

Example conditions
- Trauma
- Malignancy- pancoast tumour
- Idiopathic - Parsonage turner syndrome (brachial neuritis)

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11
Q

What would C5 radiculopathy present as

A

Weakness= shoulder abduction
Sensory loss= lateral shoulder
Reflex= reduced biceps reflex

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12
Q

What would C6 radiculopathy present as

A

Weakness= elbow flexion and wrist extension
Sensory loss= lateral forearm and thumb
Reflex= reduced brachioradialis reflex

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13
Q

What would C7 radiculopathy present as

A

Weakness= elbow extension
Sensory loss= middle finger
Reflex= reduced triceps reflex

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14
Q

What would L4 radiculopathy present as

A

Weakness= knee extension
Sensory loss= medial lower leg
Reflex= reduced patellar reflex

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15
Q

What would L5 radiculopathy present as

A

Weakness= dorsiflexion, toe extension
Sensory loss= dorsum of the foot
Reflex= intact or slightly reduced

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16
Q

What would S1 radiculopathy present as

A

Weakness= plantarflexion
Sensory loss= lateral foot
Reflex= reduced achilles reflex

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17
Q

Explain Erb’s palsy

A

Mechanism= birth trauma or shoulder traction

Weakness= shoulder abduction, elbow flexion

Posture= waiter’s tip, arm adducted, internally rotated and pronated forearm

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18
Q

Explain Klumpke’s palsy

A

Mechanism= hyperextension of the arm or traction during delivery

Weakness= intrinsic hand muscles C8-T1

Symptoms= claw hand deformity, possibly Horner’s syndrome

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19
Q

A patient presents with weakness in elbow flexion, wrist extension and sensory loss over the lateral forearm and thumb.

Which nerve root is affected?

A

C6 radiculopathy

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20
Q

What is the difference between radiculopathy and plexopathy?

A

Radiculopathy
- Follows a specific dermatome/myotome
- Pain is prominent and radiates along the dermatome
- Reflexes specific to the affected root are diminished

Plexopathy
- Involves multiple dermatomes and myotomes
- Pain may be diffuse and severe
- Associated with history of trauma, malignancy or systemic diseases

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21
Q

Differentials for focal weakness

A

Neurological
- Motor neurone disease (presents focally initially)
- Multiple sclerosis
- Peripheral nerve lesions
- Stroke/ischaemic attack
- Spinal cord lesion
- Mononeuropathies

Muscular
- Trauma
- Tumors (rhabdomyosarcoma)

Systemic
- Myasthenia gravis (ocular)

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22
Q

Differentials for generalised weakness

A

Neurological
- Motor neurone disease= amyotrophic lateral sclerosis and primary lateral sclerosis
- Multiple sclerosis
- Peripheral neuropathy= guillain barre, diabetic polyneuropathy
- Neuromyelitis optica

Muscular
- Muscular dystrophies- duchenne, myotonic
- Inflammatory= polymyositis, dermatomyositis
- Metabolic= mitochondrial myopathy and glycogen storage disorders

Systemic
- Electrolyte imbalances
- Endocrine= hypothyroidism, cushing’s
- Infections- botulism
- Toxins= organophosphates or heavy metals

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23
Q

Differentials for in-coordination (ataxia)

A

Neurological
- Cerebellar strokes
- Cerebellar abscess
- Multiple sclerosis
- Alcoholic neuropathy
- Vitamin B12 deficiency
- Friedreich’s ataxia
- Spinocerebellar ataxia

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24
Q

Differentials for imbalance

A

Muscular dystrophies
- Becker

Severe arthritis

Systemic causes
- Alcohol intoxication
- Metabolic disturbances (hypoglycaemia, electrolyte imbalance)
- Toxins or medications

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25
Q

Types of neurological gait disturbances

A

Wide-based gait- cerebellar ataxia
Shuffling gait- parkinson’s
Steppage gait- due to foot drop in peripheral neuropathy
Spastic gait- stiff, scissor like walking seen in upper motor neurone disease
Waddling gait- muscular dystrophy

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26
Q

Differential diagnoses for involuntary movements?

A

Tremors
- Resting tremor= parkinson’s
- Essential tremor- worsens with voluntary movement, may improve with alcohol
- Cerebellar tremor- intention tremor, worsens when the target is approached.
- Physiological (anxiety, caffeine)
- Dystonic tremor- irregular and posturally dependent

Chorea
- Huntington’s
- Sydenham’s- post-streptococcal autoimmune
- Lupus related chorea
- Drug induced- levodopa

Myoclonus
- Physiological myoclonus- normal jerks in sleep
- Epileptic myoclonus- juvenile myoclonic epilepsy

Dystonia
- for example cervical dystonia
- Brain injury

Tics
- Tourette’s syndrome
- Transient tic disorder

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27
Q

Differential diagnoses for faecal/urinary incontinence

A

Neurological
- Cauda equina
- Spinal cord trauma
- Multiple sclerosis
- Spinal cord tumours
- Parkinson’s
- Stroke
- Normal pressure hydrocephalus
- Dementia
- Diabetic neuropathy
- Guillain barre syndrome

Structural
- Pelvic organ prolapse
- BPH
- Urethral or anal stricture

Functional and age related causes
- Age-related degenerative changes
- Stress incontinence
- Overactive bladder syndrome

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28
Q

Is monocular diplopia neurological?

A

No
If it is binocular then it is neurological

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29
Q

What is the difference between monocular double vision and binocular double vision?

A

Monocular double vision is when double vision occurs when one eye is open

Binocular double vision only occurs when both eyes are open

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30
Q

What are the differentials for problems with vision or double vision

A

Neurological causes
Double vision
Binocular= dysfunction of cranial nerves
Monocular- problem with the eye itself
Visual field defects
Optic neuritis

Ocular causes
- Strabismus
- Orbital cellulitis
- Grave’s orbitopathy
- Diabetic retinopathy
- AMD
- Retinal vein occlusion
- Retinal detachment
- Glaucoma
- Cataracts
- Keratoconus (thinning and distortion of the cornea)
- Vitreous haemorrhage

Systemic causes
- Hypertensive retinopathy
- Temporal arteritis
- Toxic neuropathy

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31
Q

Differentials for speech and language disturbances

A

Neurological
- Stroke- brocas, wernickes and global aphasia
- Traumatic brain injury
- Multiple sclerosis
- Parkinson’s’ (reduced volume and monotone)
- Cerebellar lesions- ataxic dysarthria, slurred speech
- Friedreich’s ataxia

Dysphagia
- Stroke
- Parkinsons
- ALS
- MS

Intracranial lesions
- Stroke
- Brain tumours
- MS

Cranial nerve palsies

Non-neurological
- Functional speech disorders- psychological stress= mutism, aphonia
- Structural= laryngeal lesions, glottic lesions

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32
Q

Differential diagnoses for bulbar symptoms

A
  • Brainstem stroke (medullary)
  • MND- progressive bulbar palsy, amyotrophic lateral sclerosis
  • Myasthenia gravis
  • Guillain-Barre
  • Polymyositis/Dermatomyositis

Structural
- Brainstem tumours
- Pharyngeal pouch
- Achalasia
- Foreign body
- Oesophageal cancer/stricture

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33
Q

What are some symptoms of a brainstem stroke affecting the medulla?

A
  • Dysarthria
  • Dysphagia
  • Tongue weakness
  • Palatal weakness
  • Hoarseness
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34
Q

Differential diagnoses for cognitive dysfunction

A

Neurological
- Frontal lobe lesions- stroke, tumours, abscess, TB
- Brainstem strokes- posterior circulation, coma, locked-in syndrome
- Normal pressure hydrocephalus
- Vascular dementia
- Fronto temporal dementia

Congenital
- Down syndrome
- Tuberous sclerosis
- Fragile X syndrome

Metabolic
- Hypoxia
- Hypoglycaemia
- Hyponatremia
- Opioid overdose
- Benzodiazepines

Infectious
- Meningitis
- Encephalitis

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35
Q

Differential diagnoses for changes in behaviour/personality

A

Neurological
- Frontal lobe lesions (stroke, tumours, brain injury)
- Frontotemporal dementia
- Vascular dementia
- Huntington’s disease- irritability, aggression
- Brainstem lesions

Psychiatric
- Schizophrenia- disorganised thoughts, hallucinations
- PTSD
- Depression
- Alcohol use disorder
- Encephalopathy

Metabolic
- Hypothyroidism
- B12 deficiency- memory loss, mood changes

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36
Q

Differential diagnoses for headaches

A

Primary headaches
- Migraine- unilateral, throbbing, nausea, photophobia or phonophobia
- Tension type headache- band like pressure
- Cluster- severe, unilateral, orbital pain, lacrimation

Secondary
- Thunderclap- SAH
- ICP- visual disturbances, worse when lying down
- Low intracranial pressure- CSF leak, worse after lumbar puncture
- SOL- tumours, abscesses, worse in the morning
- Epilepsy- headache occurring after a seizure

Vascular
- SAH
- GCA
- Stroke

Infectious
- Meningitis
- Encephalitis
- Sinusitis

Systemic
- Dehydration
- Toxins- medication overuse, antiepileptic drugs

Structural
- TMJ
- Eye strain
- Glaucoma

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37
Q

Differentials for neuropathic pain syndrome

A

Peripheral
- Post-herpetic neuralgia
- Trigeminal neuralgia
- Diabetic neuropathy
- Non-diabetic causes- vitamin B12, B1 or folate deficiency, alcohol, chemo, HIV, lyme disease, Charcot-marie tooth disease
- Entrapment- carpal tunnel, ulnar

Central
- Central post stroke pain
- MS
- Spinal cord injury
- Syringomyelia (fluid filled cyst in the spinal cord)
- Neuropathic pain in Parkinson’s

Other
- Cancer related neuropathy - chemo (platinum agents, taxanes)
- Vasculitis
- Charcot-Marie-tooth disease

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38
Q

Differential diagnoses for sensory disturbance

A

Central
- Stroke= cortical, brainstem
- Multiple sclerosis
- Spinal cord lesions
- Cauda equina syndrome
- Tumours= primary CNS= glioma, meningioma

Peripheral
- Diabetic retinopathy
- Vitamin B12, B1
- Charcot-marie tooth disease
- Toxic neuropathies= alcohol, heavy metals, chemo
- Infectious neuropathies= HIV, lyme disease

Radiculopathy
- Sciatica
- Cervical/lumbar

Entrapment
- Carpal tunnel
- Ulnar neuropathy
- Meralgia paraesthetica= compressino of the lateral femoral cutaneous nerve

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39
Q

Differential diagnoses for transient motor/sensory changes

A

Central
- TIA- often associated with amaurosis fugax
- Multiple sclerosis
- Migraine with aura
- Epilepsy
- Functional neurological disorder

Peripheral
- GBS- initial stage
- Peripheral nerve compression
- Hypoglycaemia

Other
- Hyperventilation
- B12
- Transient nerve ischaemia= saturday night palsy

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40
Q

Differential for blackouts or loss of consciousness

A

Central
- Brainstem stroke
- Epilepsy- generalised tonic-clonic, focal seizures with impaired awareness, abscence seizures
- Trauma to the head

Peripheral
- Vasovagal syncope- transient autonomic dysfunction causing hypotension and bradycardia
- Cardiac syncope
- Postural hypotension
- Hypoglycaemia- inadequate glucose supply to the brain

Other
- Intoxication or drug overdose
- Hyperventilation syndrome
- Anaemia or severe hypoxia
- Severe pain or emotional distress- vasovagal response

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41
Q

What is the definition of epilepsy?

A

Epilepsy is defined as having two or more unprovoked seizures.

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42
Q

When should an EEG be done?

A

Within the first 24-48 hours of a seizure

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43
Q

What are the essential features from the history that suggest a seizure?

A
  • Aura
  • Loss of consciousness
  • Involuntary movements- jerking, tongue-biting or automatisms
  • Urinary/fecal incontinence
  • Postictal confusion and soreness after the seizure
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44
Q

Why is an EEG useful?

A

The keg diagnostic test in the evaluation of epilepsy
- Confirm diagnosis, spikes, sharp waves
- Helps distinguish between focal and generalized seizures
- Monitor treatment efficacy

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45
Q

How to investigate epilepsy

A

Clinical diagnosis

Blood tests
- Metabolic/systemic causes

EEG
- Can confirm seizure type and sometimes pinpoint seizure focus

Imaging
- MRI- checks for structural abnormalities in the brain (scarring, tumours, strokes)

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46
Q

What is the difference between generalized and focal seizures?

A

Generalized
- Involves both hemispheres of the brain
- Examples include tonic-clonic seizures and absence seizures

Partial
- Begin in one specific part of the hemisphere
- Localized twitching, sensory changes or altered awareness.

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47
Q

What are the three types of seizures that occur in primary generalised epilepsy?

A
  • Myoclonus
  • Generalised tonic clonic seizures
  • Absence seizures
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48
Q

How can you tell the difference between primary generalised seizures and secondary generalized seizures?

A

Primary= affects both hemispheres of the brain from the start.

Secondary= Focal onset that progresses to tonic-clonic. Starts in one part of the brain but spread to both hemispheres.

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49
Q

Typical features and management for primary generalized seizures

A
  • Affects both hemispheres from the start
  • Loss of consciousness
  • Tonic-clonic, abscence or atonic seizures

Management
- AEDs: Sodium valproate, lamotrigine and levertiracetam
- Lifestyle modifications= avoid triggers (alcohol), ensure good sleep
- Referral to a neurologist for diagnosis and treatment adjustment.

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50
Q

Features and management of secondary generalized seizures

A
  • Starts as a focal seizure with symptoms like sensory changes, jerking or auras (deja vu, smells)
  • Progresses to tonic-clonic with loss of consciousness and convulsions
  • Postictal confusion often follows

Management
- AEDs- carbamazepine, lamotrigine
- Treat underlying causes (lesions, infections)

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51
Q

Features and management of absence seizures

A
  • Common in children
  • Brief episodes (5-20 seconds) of staring
  • No awareness of surroundings but no fall
  • May involve subtle eye blinking or eye smacking
  • No postictal confusion

Managment
- First line= Ethosuximide (Zarontin), valproate
- Avoid triggers- flashing lights, hyperventilation

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52
Q

What is the first line treatment for absence seizures?

A

Ethosuximide (Zarontin)

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53
Q

Clinical features and management of focal aware (simple partial seizures)

A
  • Person remains fully aware
  • Motor symptoms= localized jerking (face, arm and leg)
  • Sensory symptoms= tingling, numbness or unusual sensations
  • Autonomic symptoms= sweating, flushing or palpitations
  • Psychic symptoms- Deja vu, fear or hallucinations

Management
- AEDs= carbamazepine, lamotrigine

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54
Q

Clinical features and management of focal impaired awareness (complex partial seizures)

A
  • Starts in one area of the brain but affects awareness
  • Aura may precede
  • Person appears confused or unresponsive
  • Automatism- repetitive movements like lip-smacking, chewing or picking at clothes
  • May wander aimlessly

Management
- Carbamazepine, levertiracetam, lamotrigine
- Consider surgery if focal seizures are drug resistant

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55
Q

Management advice to give to a patient and their relative about epilepsy?

A

Medication adherence and safety- side effects, medical alert bracelet.

Identifying and managing triggers- lack of sleep, stress, alcohol or flashing lights

Lifestyle and health
- Regular sleep schedule, balanced diet, manage stress to minimise seizure risks

Work, recreation and safety
- Grab bars, padded furniture

Contraception, pregnancy and first aid

Relatives- be aware of the signs of a seizure, stay calm and don’t put anything in their mouth

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56
Q

DVLA and epilepsy- first unprovoked/isolate seizure

A

6 months off if there are no relevant structural abnormalities on brain imaging and no definite epileptiform activity on EEG

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57
Q

DVLA and epilepsy- established epilepsy

A

Can drive if they have been seizure free for 12 months

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58
Q

DVLA and withdrawal of epilepsy medication

A

Should not drive whilst anti-epilepsy medication is being withdrawn and for 6 months after the last dose

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59
Q

What are 5 causes of secondary epilepsy?

A

Traumatic brain injury
Stroke
Brain tumors
Infections- meningitis, encephalitis
Genetic disorders or metabolic imbalances- hypoglycaemia, neurofibromatosis

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60
Q

What anti-epileptic drugs do you have to do blood monitoring for?

A
  • ## Sodium valproate (LFTs, platelet/ammonia levels, valproate levels)
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61
Q

What anti-epileptic drug can lead to Stevens Johnson syndrome?

A

Lamotrigine and carbamazepine

62
Q

What anti-epileptic medication is contra-indicated in pregnant women?

A

Sodium valproate

63
Q

General side effects of all anti-epileptic drugs

A
  • Drowsiness
  • Fatigue
  • Dizziness
  • Nausea
64
Q

Clinical manifestations of a tension headache

A

At least two of the following:

  • Bilateral location
  • Pressing or tightening
  • Mild or moderate intensity
  • Not aggravated by routine physical activity

No nausea or vomiting and
No more than one of photophobia or phonophobia

65
Q

What is the management for tension headaches?

A

Episodic
- Paracetamol, NSAIDs
- Stress, anxiety help

Chronic
- Acupuncture
- Low dose amitriptyline- aim to wean off after 4-6 months.
- Referral to neurology if there is no improvement

66
Q

What are the characteristics of a migraine

A
  • Unilateral pulsating headache accompanied by symptoms like nausea and vomiting, photophobia and phonophobia.
  • Last 4-72 hours
67
Q

What defines a chronic migraine?

A

Headache on more than 15 days of each month, 8 of which have features of migraine

68
Q

What is the ICHD-3 criteria for a migraine?

A
  1. At least five attacks fulfilling criteria 2-4
  2. Headache attacks lasting 4-72 hr (untreated or unsuccessfully treated)
  3. Headache has at least two of the following four characteristics:
    unilateral location
    pulsating quality
    moderate or severe pain intensity
    aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)
  4. During headache at least one of the following:
    nausea and/or vomiting
    photophobia and phonophobia
  5. Not better accounted for by another ICHD-3 diagnosis.
69
Q

What is the treatment for migraines?

A

Acute
- NSAIDs (e.g., ibuprofen or naproxen)
- Paracetamol
- Triptans (e.g., sumatriptan)
- Antiemetics if vomiting occurs (e.g., metoclopramide or prochlorperazine)

Prophylaxis
- Propranolol (a non-selective beta blocker)
- Amitriptyline (a tricyclic antidepressant)
- Topiramate (teratogenic and very effective contraception is needed, anti-epileptic medication)

70
Q

How do Triptans work with migraines?

A

Serotonin agonists (5-HT)

  • Cranial vasoconstriction
  • Inhibits inflammatory and pain signals

Do not take a second dose

71
Q

What is the management for medication overuse headaches?

A

Management (from 2008 SIGN guidelines)
simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)
opioid analgesics should be gradually withdrawn

There is no physical dependence for simple analgesics so they can be stopped suddenly

72
Q
A
72
Q

Complications of medication overuse headaches

A

Withdrawal symptoms such as vomiting, hypotension, tachycardia, restlessness, sleep disturbances and anxiety may occur when medication is stopped

73
Q

Characteristics of cluster headaches

A
  • Severe unilateral orbital/temporal pain
  • Miosis
  • Ptosis
  • Nasal discharge
  • Eyelid oedema
  • Lasts 15-180 minutes
74
Q

How to diagnose a cluster headache

A

The following diagnostic criteria are given:

At least five attacks fulfilling criteria B-D
Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 minutes (when untreated)
Either or both of the following:
at least one of the following symptoms or signs, ipsilateral to the headache:
- conjunctival injection and/or l– - - lacrimation
- nasal congestion and/or rhinorrhoea
- eyelid oedema
- forehead and facial sweating
- miosis and/or ptosis
- a sense of restlessness or agitation
Occurring with a frequency between one every other day and 8 per day
Not better accounted for by another ICHD-3 diagnosis.

75
Q

Acute management of cluster headaches?

A

Treatment options during acute attacks are:

Triptans (e.g., subcutaneous or intranasal sumatriptan)
High-flow 100% oxygen (may be kept at home)

76
Q

First line prophylaxis for cluster headaches

A

Verapamil

77
Q

Causes of spontaneous subarahncoid haemorrhage

A

Intracranial aneurysm (saccular ‘berry’ aneurysms)
accounts for around 85% of cases

conditions associated with berry aneurysms include

  • hypertension
  • adult polycystic kidney disease
  • Ehlers-Danlos syndrome
  • coarctation of the aorta
  • arteriovenous malformation
  • pituitary apoplexy
  • mycotic (infective) aneurysms
78
Q

Where is the subarachnoid space found?

A

Between the arachnoid and pia mater

79
Q

Symptoms and signs of subarachnoid haemorrhages

A

Symptoms
Headache (97% of cases)
Photophobia
Neck stiffness
Nausea
Vomiting

Signs
Neck stiffness
Cranial nerve palsy (e.g. third nerve palsy)
Reduced consciousness (coma)
Diplopia (double vision)
Ptosis

80
Q

Complications of subarachnoid haemorrahge

A

Vasospasm, rebleeding, hydrocephalus, death.

81
Q

Management of subarachnoid haemorrahge

A
  • Stabilization
  • Neurosurgical intervention (clipping/coiling aneurysm)
  • Blood pressure control
  • Nimodipine to prevent vasospasm.
82
Q

When should you do a lumbar puncture after a subarachnoid haemorrhage and what would you see?

A

Should be delayed for 12 hours since symptom onset. When there is a normal CT head.

Opening pressure: elevated in SAH

  • Red cell count: elevated in SAH. May be seen in a traumatic LP. Sequential tubes (e.g. 1-4) can be taken to look for a fall in red blood cell concentration. A traumatic LP is supported by a significant reduction in red cells between the first and last tubes.
  • Xanthochromia (visual inspection): a breakdown product of haemoglobin. May be detected visually. At 12 hours post-SAH, 100% of patients will have xanthochromia. Lasts for ~2 weeks.
  • Bilirubin (spectrophotometry): spectrophotometry detects blood breakdown products, in particular, bilirubin. More sensitive than visual inspection. Samples must be protected from light and sent immediately to the laboratory for analysis. Lasts for ~4 weeks (if extensive bleed).
83
Q

Hydrocephalus is a complication of a subarachnoid haemorrahge. What is the management of this?

A

Hydrocephalus refers to increased cerebrospinal fluid, causing expansion of the ventricles. Treatment options include:

Lumbar puncture
External ventricular drain (a drain inserted into the brain ventricles to drain CSF)
Ventriculoperitoneal (VP) shunt (a catheter connecting the ventricles with the peritoneal cavity)

84
Q

What is cushing’s triad?

A

Cushing’s reflex is a physiological response to raised intracranial pressure, which causes hypertension, bradycardia and irregular respirations (Cushing’s triad). It is a late sign and suggests impending brainstem herniation.

85
Q

Characteristics of a space occupying lesion

A
  • Dull
  • Constant
  • Bilateral
  • Seizures
  • Postural
  • Papilloedema
  • Vomiting
  • Focal neurological deficits- weakness, sensory changes, aphasia and visual deficits
86
Q

Diagnosis of space occupying lesion

A

CT/MRI with contrast

87
Q

Medications for a space occupying lesion

A

Medications: steroids for vasogenic oedema (e.g. dexamethasone), proton pump inhibitors (gastric protection) and anti-seizure medication (e.g. levetiracetam)

88
Q

Characteristics of meningitis

A
  • Fever
  • Headache
  • Photophobia
  • Neck stiffness
  • Altered mental state
  • Meningococcal rash
  • Seizures
89
Q

Non-infectious causes of meningitis

A

Non-infectious causes include malignancy, systemic inflammatory conditions (e.g. systemic lupus erythematous, Behçet’s disease), head injury, medications (e.g. NSAIDs, co-trimoxazole) or surgery.

90
Q

What are complications of meningitis?

A
  • Sensorineural hearing loss is a key complication
  • Seizures and epilepsy
  • Cognitive impairment and learning disability
  • Memory loss
  • Cerebral palsy, with focal neurological deficits such as limb weakness or spasticity
91
Q

If you have been in contact with someone with meningitis 7 days from initial symptoms, what management should you have?

A

Post exposure prophylaxis
Single dose of ciprofloxacin
Ideally within 24 hours of the initial diagnosis

92
Q

If you suspect meningitis in a child in the community, what is the management?

A

urgent stat injection (IM or IV) of benzylpenicillin prior to transfer to hospital

suspected meningitis and a non-blanching rash

93
Q

Under what circumstances should you delay lumbar puncture?

A

Lumbar puncture should be delayed in the following circumstances
signs of severe sepsis or a rapidly evolving rash
severe respiratory/cardiac compromise
significant bleeding risk
signs of raised intracranial pressure
focal neurological signs
papilloedema
continuous or uncontrolled seizures
GCS ≤ 12

94
Q

Management of idiopathic intracranial hypertension?

A

Acetazolamide

95
Q

Features of idiopathic intracranial hypertension

A

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

96
Q

Overall management for idiopathic intracranial hypertension

A

Conservative: weight loss, discontinue causative medications.
Medical: acetazolamide (first-line), topiramate, furosemide.
Therapeutic serial lumbar punctures (temporary measure).
Surgical: CSF diversion procedures (ventriculoperitoneal shunt preferred), optic nerve sheath fenestration (ONSF).

97
Q

What are some complications of idiopathic intracranial hypertension?

A

Permanent visual loss, especially in advanced disease; urgent surgical referral for severe cases.

98
Q

Signs of GCA

A

Abnormal temporal artery: typically thickened, tender with reduced or absent pulse

Scalp tenderness on palpation

Transient or permanent visual loss

Visual field defects

Optic disc changes: pale, swollen optic disc (anterior ischaemic optic neuritis)

Retinal changes: pale retina with cherry red spot (central retinal artery occlusion)

Other: cranial nerve palsies, asymmetrical pulses (if large vessel involvement - subclavian)

99
Q

4 types of injuries that can come from traumatic brain injuries

A
  • Extradural haematoma
  • Subdural haematoma
  • Subarachnoid haemorrhage
  • Intracerebral haemorrhage
100
Q

Characteristics of post-traumatic headache

A
  • Dull
  • Tension like
  • Dizziness
  • Mood changes
  • Cognitive issues
101
Q

Management of post-traumatic headache

A
  • NSAIDs
  • Amitryptyline
  • Physiotherapy
  • Psychological therapy
102
Q

First line for acute bacterial sinusitis

A

Phenoxymethylpenicillin

103
Q

When performing a lumbar puncture, what should you always consider?

A

Measuring CSF opening pressure using a manometer

104
Q

What are clinical circumstances in which CSF examination may be helpful?

A
  • Suspected subarachnoid haemorrhage
  • Suspected meningitis/encephalitis
  • Immunological disorders such as multiple sclerosis or GBS
105
Q

Three key points for CSF results from bacterial meningitis

A

Cloudy appearance: Due to high WBC count and proteins.
Markedly elevated protein: Often >100 mg/dL.
Low glucose: Typically <40 mg/dL due to bacteria consuming glucose.

106
Q

Three key points for CSF results from viral meningitis

A

Clear appearance: Unlike bacterial, it’s usually clear.
Moderate lymphocytic pleocytosis: Lymphocytes dominate the white cells.
Normal or mildly low glucose: Usually >40 mg/dL (not as low as in bacterial meningitis).

107
Q

Three key points for CSF results from TB meningitis

A

Slightly cloudy appearance: More subtle than bacterial, but not clear.
Marked protein elevation: Often >100 mg/dL, higher than viral.
Low glucose: Like bacterial meningitis, glucose is usually <40 mg/dL.

108
Q

Three key points for CSF results from TB meningitis

A

Xanthochromic (yellow) fluid: Due to RBC breakdown, this is the key feature.
Elevated opening pressure: Common due to the bleed.
Red blood cells (RBCs): Presence of RBCs without trauma to the needle; suggests bleeding into the subarachnoid space.

109
Q

Three key points for CSF results from TB meningitis

A

Clear appearance: No infection or hemorrhage, so the fluid looks normal.
Markedly elevated protein: High protein (often >100 mg/dL) but normal white cells — classic albuminocytologic dissociation.
Normal glucose: Unlike infections, glucose stays normal in GBS.

110
Q

Are neurodegenerative conditions normally asymmetric or symmetric in the early stages?

A

Asymmetric

111
Q

How do you diagnose idiopathic parkinson’s disease

A

Step 1. Diagnosis of Parkinsonian Syndrome:
* Bradykinesia
* At least one of the following
o Muscular rigidity
o 4-6 Hz rest tremor
o postural instability not caused by primary visual, vestibular, cerebellar, or proprioceptive dysfunction
Step 2. Exclusion of other causes of parkinsonism.
Step 3. Supportive prospective positive criteria for Parkinson’s disease
Three or more required for diagnosis of definite Parkinson’s disease in combination with step one:

  • Unilateral onset
  • Rest tremor present
  • Progressive disorder
  • Persistent asymmetry affecting side of onset most
  • Excellent response (70-100%) to levodopa
  • Severe levodopa-induced chorea
  • Levodopa response for 5 years or more
  • Clinical course of ten years or more
112
Q

What is a festinating gait?

A

Rapid frequency of steps to compensate for the small steps and avoid falling (“festinating” gait)

113
Q

How can you stage Parkinson’s disease?

A

Hoehn and Yahr scale and the unified parkinson’s disease rating scale

114
Q

Mode of action and major side effects of Levodopa

A

Mode of Action:
- Levodopa is a dopamine precursor converted to dopamine in the brain.
- Carbidopa/Benserazide inhibits peripheral conversion of Levodopa to dopamine, increasing central availability.

Major Side Effects:
- Nausea and vomiting
- Dyskinesias (involuntary movements) with long-term use
- Motor fluctuations (“on-off” phenomena)
- Orthostatic hypotension
- Hallucinations and confusion (especially in elderly)

115
Q

Examples of dopamine agonists, mode of action and major side effects

A

Ropinirole, pramipexole, rotigotine

Stimulate dopamine receptors directly in the brain

Major side effects
- Nausea and vomiting
- Orthostatic hypotension
- Impulse control disorders- gambling, hypersexuality, compulsive shopping
- Daytime sleepiness and sudden sleep attacks
- Hallucinations and confusion

116
Q

Example of monoamine oxidase B inhibitors, mode of action and major side effects

A

Selegiline and rasagiline

Inhibits the breakdown of dopamine by blocking MAO-B enzyme activity

Major side effects
- Nausea
- Insomnia (especially with selegiline)
- Headaches
- Hallucinations rare

117
Q

Example of COMT inhibitors, mode of action and major side effects

A

Entacapone and Tolcapone

Inhibits COMT enzyme, reducing the breakdown of Levodopa, then prolonging its effects

Major side effects
- Diarrhoea
- Orange discoloration of urine
- Dyskinesias
- Hepatotoxicity

118
Q

Summarise non-oral treatments for IPD

A

Apomorphine (Subcutaneous Infusion or Injections)

Mode of Action: Dopamine agonist providing rapid symptomatic relief.
Indications: For patients with severe motor fluctuations or “off” episodes.
Administration: Delivered as a continuous subcutaneous infusion via a pump or intermittent injection.
Side Effects: Nausea, orthostatic hypotension, site reactions, somnolence.
Levodopa-Carbidopa Intestinal Gel (Duodopa)

Mode of Action: Continuous infusion of Levodopa via a percutaneous gastrojejunostomy tube.
Indications: For advanced Parkinson’s with severe motor fluctuations and dyskinesias.
Side Effects: Site infections, tube dislodgment, nausea, dyskinesias.
Deep Brain Stimulation (DBS)

Mode of Action: High-frequency electrical stimulation of the subthalamic nucleus (STN) or globus pallidus internus (GPi), which modulates motor pathways.
Indications: For advanced Parkinson’s with motor complications not adequately controlled by medications.
Side Effects: Surgical risks (e.g., infection, hemorrhage), speech difficulties, cognitive decline in some cases.
Botulinum Toxin Injections

Mode of Action: Blocks acetylcholine release at the neuromuscular junction to reduce dystonia or tremors.
Indications: For focal dystonia, excessive drooling (sialorrhea), or tremor.
Side Effects: Local weakness, discomfort at the injection site.

119
Q

Who is in the multidisciplinary team for IPD?

A
  • Medical specialist (Neurologist or Geriatrician)
  • PD specialist nurse
  • Physiotherapist
  • Occupational therapist
  • Speech and Language Specialist
  • Dietician (later stages)
  • Psychiatrist (sometimes
120
Q

What are the 4 distinct phases of IPD

A
  1. Early stage - Soon after diagnosis, symptoms are mild and normal life possible
  2. Maintenance stage - Good response to treatment and no major disability
  3. Advanced stage - Poor response to drugs with motor side effects
  4. Palliative stage - Unable to live independently and in need of multidisciplinary support
121
Q

What are severe complications of advanced IPD

A

Aspiration Pneumonia: From dysphagia and poor cough reflex.

Immobilization Complications: Pressure ulcers, infections, and venous thromboembolism (VTE).

Social Isolation and Caregiver Burden: Due to increasing dependency.

122
Q

Complications seen in advancing IPD

A

Motor Complications
Motor Fluctuations

Wearing-off phenomena: Symptoms return as the effect of Levodopa wears off between doses.
On-off phenomena: Unpredictable periods of mobility (“on”) and immobility (“off”).
Freezing of gait: Sudden inability to move, often triggered by specific circumstances.
Dyskinesias

Involuntary movements (e.g., chorea or dystonia) due to long-term Levodopa use.
Postural Instability

Increased risk of falls and injuries as balance deteriorates.
Axial Symptoms

Progressive difficulties with speech (dysarthria), swallowing (dysphagia), and posture (camptocormia, Pisa syndrome).
Non-Motor Complications
Cognitive Decline

Mild cognitive impairment or progression to Parkinson’s Disease Dementia (PDD).
Neuropsychiatric Symptoms

Depression, anxiety, apathy, hallucinations, and delusions (often medication-related).
Autonomic Dysfunction

Orthostatic hypotension, urinary incontinence, constipation, sexual dysfunction, and excessive sweating.
Sleep Disturbances

Insomnia, REM sleep behavior disorder, and excessive daytime sleepiness.
Pain and Sensory Symptoms

Musculoskeletal pain, neuropathic pain, or dystonic pain.

123
Q

What characteristics are not involved in MND?

A
  • Sensory pathways
  • Special senses
  • Micturition (spares the autonomic nervous system)
124
Q

How is the diagnosis of MND confirmed?

A

Confirmed using electromyography

125
Q

How can the rate of progression of MND be slowed?

A

Riluzole (a glutamate inhibitor)

126
Q

What is the average survival time of MND?

A

3 years

127
Q

What are the clinical variants of MND?

A
  • Amyotrophic lateral sclerosis
  • Progressive bulbar palsy
  • Progressive muscular atrophy (LMN) rare
  • Progressive lateral sclerosis (UMN) rare
128
Q

Clinical features of amyotrophic lateral sclerosis

A
  • Typically LMN signs in arms and UMN signs in legs
  • Often starts in one limb (difficulty with grip or foot drop)
129
Q

Clinical features of progressive bulbar palsy

A
  • Mainly bulbar symptoms
  • Slurred or nasal speech
  • Difficulty swallowing
  • Weakness of tongue and facial muscles
  • Carries worst prognosis
130
Q

Describe what type of respiratory failure you get with motor neurone disease?

A

Type 2 respiratory failure
Hypercapnic respiratory failure

Management is with non-invasive ventilation- Bilevel positive airway pressure used at night
Survival benefit of around 7 months

131
Q
A
131
Q

How do you manage dysphagia in MND

A

Percutaneous gastrostomy tube is the preferred way to support nutrition and has been associated with prolonged survival

132
Q

Does multiple sclerosis affect the peripheral nervous system?

A

MS is an acquired, immune-mediated inflammatory, demyelinating, condition that affects both the brain and spinal cord.

133
Q

What are the 3 main patterns of clinical presentation of multiple sclerosis

A
  • Relapsing-remitting- early stages, symptoms may completely remit. As diseases progresses likely to retain residual damage with each relapse.
  • Primary progressive- may have periods where disease is not active or non-progressive, but no clinical remission
  • Secondary progressive= gradual, sustained worsening in neurological function. Without remission
134
Q

What optic neuritis presents as

A
  • Central scotoma
  • Pain with eye movement
  • Impaired colour vision
  • Relative afferent pupillary defect
135
Q

How does trigeminal neuralgia present in MS?

A
  • Severe stabbing facial pain
  • Sudden, brief, severe and electric shock like pain that lasts seconds to minutes.
  • Unilateral or bilateral pain
136
Q

What are the investigations in MS?

A
  1. MRI of brain or spinal cord - will demonstrate demyelination plaques
  2. Immunoelectrophoresis of CSF - will show oligoclonal bands of IgG
137
Q

How to treat multiple sclerosis in a acute relapse?

A

IV methylprednisolone may be given for 5 days

138
Q

Examples of drugs used to reduce the risk of relapse of MS?

A
  • Natalizumab
  • Ocrelizumab
  • Fingolimod
139
Q

Differential diagnoses for multiple sclerosis

A

Metabolic Diseases:
- Vitamin B12 Deficiency – Causes subacute combined degeneration, with macrocytic anemia.
- Diabetic Neuropathy – Symmetric distal neuropathy, no CNS lesions.
- Adult-Onset Leukodystrophies – Progressive white matter changes, genetic disorders.
- Copper Deficiency – Myelopathy with low serum copper, linked to malabsorption.

Demyelinating Diseases:
- Neuromyelitis Optica – Affects optic nerves and spinal cord, associated with AQP4 antibodies.
- Transverse Myelitis – Single spinal cord lesion, no dissemination in time or space.
- Acute Disseminated Encephalomyelitis – Post-infectious, monophasic, with acute encephalopathy.

Infections:
- Lyme Disease – Associated with tick exposure, can cause cranial nerve palsies.
- Human T-Lymphotropic Virus (HTLV-1) – Causes progressive spastic paraparesis, tested with HTLV-1 serology.
- Tertiary Syphilis – Tabes dorsalis, painless sensory loss, syphilis serology.

140
Q

Medication and interventions to help with spasticity in multiple sclerosis

A

Baclofen (a muscle relaxant) and tizanidine (an alpha-2 adrenergic agonist) are commonly used.

Cannabinoid-based therapies like nabiximols may also help reduce spasticity and associated pai

141
Q

Medication to help with neuropathic pain

A

Gabapentin and pregabalin are first-line treatments.

Tricyclic antidepressants, such as amitriptyline, may also be beneficial​

In some cases, opioids may be used, though their long-term efficacy in MS-related pain is limited

142
Q

Medication used in depression

A

Selective serotonin reuptake inhibitors (SSRIs) such as sertraline or SNRIs like venlafaxine are commonly prescribed.

Mirtazapine may also be used for patients with fatigue and depression​

143
Q

Medication used in incontinence

A

For urinary urgency, oxybutynin (an anticholinergic) or tolterodine may be used.

Bethanechol may help with urinary retention​

144
Q

Medication used in fatigue in multiple sclerosis

A

Modafinil and amantadine

145
Q

Medication used for paroxysmal symptoms

A

Carbamazepine or oxcarbazepine (anti-epileptic drugs) can be effective for symptoms like trigeminal neuralgia or Lhermitte’s sign

146
Q

How does Natalizumab work for multiple sclerosis and what are some side effects?

A
  • Blocking the adhesion of immune cells to the blood-brain barrier.
  • Progressive multifocal leukoencephalopathy
147
Q

Mechanism of action and side effects of Interferon beta

A

Avonex, Betaseron
- Modify the immune response by reducing the activation of T cells
- flu like syptoms, depression.

148
Q

Mechanism of action of flatiramer acetate and side effects used for multiple sclerosis

A
  • Mimics the protective myelin protein
  • Flushing and chest pain.
149
Q

How does multiple sclerosis affect pregnancy?

A
  • Temporary reduction in disease activity during pregnancy
  • After delivery, the risk of MS relapses increases for the first 6 months
  • No significant impact on pregnancy

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