Neurology Flashcards
1
Q
Definition of Bell’s Palsy?
A
Unilateral peripheral facial nerve palsy with unremarkable physical examination and history
-Facial nerve aetiolgoy
2
Q
Which motor neurones are affected in Bell’s Palsy?
A
CN VII, lower motor neurones, affecting both contralateral and ipsilateral motor cortices
Equal distribution of facial weakness across facial zones
Note: Does not spare the forehead
3
Q
What are the symptoms of Bell’s Palsy?
A
Absence of nasolabial fold
Drooping of the eyelid and mouth
- Drooling, difficulty eating/drinking
-Keratoconjunctivitis sicca (dry eye) with parasympathetic dysfunction of the lacrimal gland
Hyperacusis
Dysgeusia- loss of taste on anterior 2/3rd of the tongue
Post-auricular pain
Symptoms fully evolve in 72 hours
4
Q
How is Bell’s Palsy diagnosed?
A
Clinical diagnosis
Consider electroneuronography - >90% decrease in compound muscle action potential.
5
Q
Which infectious diseases can cause facial nerve palsies?
A
Borella burgdorefi - Lyme disease
EBV
HSV-1
VZ
6
Q
What is the palpebral-oculogyric reflex in Bell’s Palsy?
A
• Attempted eyelid closure Upward eye deviation (when eye remains open).
7
Q
What should be examined to exclude Ramsay Hunt Syndrome in Bell’s Palsy?
A
Otoscopy - vesicular rash in the auditory canal suggests RHS.
8
Q
What is the treatment for Bell’s Palsy?
A
High dose 50mg OM Prednisolone within 72 hours of onset
Protection of the cornea with artificial tears
surgery - Lateral tarssorrhaphy is established corneal damage
9
Q
What is the management for Ramsay Hunt Syndrome?
A
Corticosteroid + Acyclovir
10
Q
What are the complications of Bells Palsy?
A
Keratoconjunctivitis Sicca
Contracture and synkinesis
Crocodile tears
11
Q
What is the definition of a cluster headache?
A
Severe headache characterised by unilateral pain persisting 15-180 minutes untreated occurring at a cyclical pattern
12
Q
What is the distribution of pain in cluster headaches?
A
Phantom of the opera mask distribution of pain pattern
13
Q
What are the symptoms of cluster headaches?
A
Conjunctival redness and/or lacramation
Nasal congestion or rhinorrhoea
Eyelid oedema
Flushing and facial swelling
14
Q
What are the risk factors for cluster headaches?
A
Male sex
Family history
Cigarette smoking and heaving drinking (+ sleep disruption)
15
Q
Which reflex is thought to be implicated in the aetiology of cluster headaches?
A
Trigeminal autonomic reflex
16
Q
Which brain structure is responsible for regulating circadian rhythms and is linked to the cyclical pattern of cluster headaches?
A
Hypothalamus
17
Q
What is the presentation of cluster headaches?
A
Forehead and facial sweating Miosis or ptosis A sense of restlessness or agitation Photophobia, phonophobia Frequency of headache 1-8-per day (diurnal pattern)
18
Q
What is the average number of daily headaches in Cluster headaches?
A
4
19
Q
What are the two types of cluster headaches?
A
Episodic
Chronic
20
Q
What are episodic cluster headaches?
A
occurring in periods lasting 7 days - separate by pain-free periods lasting a month or longer
21
Q
What are chronic cluster headaches?
A
Occurring for 1 year without remissions or with short-lived remissions of less than a month
22
Q
What is the pattern of occurrence in cluster headaches?
A
Cluster headaches last 4-12 weeks (Interval between bouts tend to be the same)
Occur once ever year or every two years - seasonal pattern
Headaches typically occur at night, 1-2 hours after falling sleep
23
Q
Describe the onset of cluster headaches?
A
10 minutes
24
Q
Describe the pain of cluster headaches?
A
Intense, sharp and penetrating centered around the eye, temple or forehead with a unilateral presentation
25
How long does a cluster headache typically last?
45-90 minutes (Range 15 minutes-3 hours)
26
What is the definition of motor neurone disease?
A neurodegenerative disorder of cortical, brain stem and spinal neurones (Lower and upper motor neurones) characterised by progressive muscle weakness
27
What is ALS?
• Amyotrophic lateral sclerosis (ALS): Combined degeneration of UMN and LMN.
28
What is progressive bulbar palsy variant of MND?
Dysarthria and dysphagia + atrophied fasciculating tongue (LMN) and brisk jaw jerk (UMN).
29
Which mutation is associated with motor neurone disease?
SOD1 mutation
30
What is the aetiology of motor neurone disease?
Free radical damage and glutamate excitotoxicity have been implicated in familial motor neurone disease
-Progressive motor neurone degeneration and death with gliosis replacing lost neurones
31
What is the presentation of motor neurone disease?
Upper limb weakness --> Difficulty with ADLs
Stiffness with poor coordination and balance
Spasticity
Dysarthria
Dysphagia
LMN signs
- painful muscle spasms
- Foot drop
- Muscle atrophy
- Slurred speech and dysphonic speech
32
What are the LMN examination features in MND?
Muscle wasting
Fasciculations
Flaccid weakness
Reduced or absent reflexes
33
What are the upper motor neurone features in MND?
Spastic weakness
Brisk reflexes
Hypertonia
Extensor plantar (Babinski's sign)
34
What investigations are performed to diagnose MND?
Electromyography (EMG)
-Features of chronic and acute denervation with giant motor unit action potentials in more than 1 limb.
MRI -used to exclude cord or root compression and brainstem lesion
35
What pharmacological therapy is implicated in the management of MND?
Riluzole
36
What is Riluzole?
Inactivator of voltage-gated sodium channels, and indirect inhibitor of glutamate release - reduces motor neurone firing and prolongs survival
37
What are the symptomatic treatment for MND?
Spasticity (baclofen), salivation (anticholinergics), dyspnoea and anxiety (opiates, benzodiazepines).
38
What are the end of life management options for MND?
End of life management
Consider percutaneous endoscopic gastrostomy (PEG) and non-invasive ventilation.
• Consider hospice care in terminal stages.
39
What are the complications associated with MND?
* Depression
* Emotional lability
* Frontal-type dementia
* Weight loss and malnutrition (resulting from dysphagia)
* Immobility-related problems: DVT, aspiration pneumonia.
40
What is the main cause of death in MND disease?
Respiratory failure because of respiratory muscle weakness
41
Define multiple sclerosis?
An inflammatory demyelinating disease of the central nervous system
42
What is the most common form of multiple sclerosis?
Relapsing-remitting MS - Characterised by clinical attacks of demyelination with complete recovery in between attacks
43
What is primary progressive MS?
Gradual accumulation of disability with no clear relapsing-remitting pattern
44
What is the aetiology of MS?
Autoimmune degeneration of CNS myelin results in impaired conduction of electrical impulses along axons
Associated grey matter atrophy and T-cell mediated phagocytosis of oligodendrocytes
45
What are the risk factors for MS?
Female Sex (Presents at 20-40 years)
Family history of MS
Genes encoding for HLA-DR2
EBV exposure
46
What is the presentation of MS?
Optic neuritis
Sensory systems
Motor - limb weakness, spasms, stiffness, heaviness (Foot dragging)
Autonomic - Urinary urgency, hesitancy, incontinence and impotence
Psychological: Depression and psychosis
Paraesthesia (Loss of vibration and join position)
47
What is optic neuritis in MS?
Unilateral deterioration in visual acuity and colour perception + pain in eye movement
48
What is Uhthoff's phenomenon?
Transient increase or recurrence of symptoms due to conduction block precipitated by a rise in body temperature
49
What is Charcot's neurological triad?
Dysarthria - Plaques in the brain stem
Nystagmus - Plaques on the optic nerve
Intention tremor - Plaques along motor pathways
50
How is optic neuritis examined in MS?
Fundoscopy revealing swollen optic nerve head (optic atrophy in chronic disease)
Visual field testing - Central scotoma (optic nerve affected) or field defects (optic radiations affected)
51
What visual abnormalities are detected on examination in MS?
Relative afferent pupillary defect
-Using swinging torch test - both pupils contract when light is shone on the unaffected side
Both pupils dilate when the light is swung go the diseased eye
Optic neuritis
Internuclear ophthalmoplegia
-Lateral horizontal gaze - Failure of adduction on the contralateral eye
52
What are the cerebellar signs in MS?
```
Limb ataxia
Intention tremor
Past-pointing
Dysmetria on finger-nose test
Dysdiadochokinesis
Ataxic wide-based gait, scanning speech
```
53
What is Lhermitte's phenomenon?
Electric shock-like sensation in arms and legs precipitated by neck flexion.
54
What are the investigations to diagnose MS?
MRI -Gadolinium contrast
-Plaque detection is highlighted as high-signal lesions
Hyperintensities in the periventricular white matter (plaques with myelin)
Diagnosis is based on two or more CNS lesions with corresponding symptoms separated in time and space (McDonald Criteria)
55
What criteria is used in the diagnosis of MS?
McDonald Criteria
56
What signs are seen on a lumbar puncture in MS?
Positive oligoclonal banding
57
What is the acute management of MS?
Corticosteroids- IV methylprednisolone
58
What is the chronic management of relapsing remitting MS?
β-Interferon or glatiramer SC injections may reduce relapse frequency.
Natalizumab (Monoclonal antibody – prevents T-cell movement into the CNS) – reduces relapse & disability progression.
Cladribine/Fingolomid – Shown to be superior to B-interferon.
59
What is the first-line management for cluster headaches?
100% oxygen, and subcutaneous triptan
60
What is the prophylaxis for cluster headaches?
Verapamil
61
What is myasthenia gravis?
An autoimmune disease affecting the post-synaptic membrane of a neuromuscular junction - resulting in weakness off skeletal muscles
62
Which antibodies are involved with myasthenia Gravis?
Nicotinic acetylcholine receptor antibodies
63
What is the paraneoplastic subtype of myasthenia Gravis?
Lambert-Eaton Myasthenic syndrome- caused by autoantibodies against presynaptic calcium ion channels
64
What is strongly associated with myasthenia gravis?
Thymoma development
65
What is the presentation of myasthenia gravis?
Progressive muscle weakness is worsened with repetitive use.
Ocular symptoms: Drooping eyelids, diplopia,
Bulbar symptoms: Facial weakness (myasthenic snarl) , disturbed hypernasal speech, difficulty in similing, chewing or swallowing
66
What is the pattern of muscle weakness with repeated use in Lambert-Eaton Syndrome?
Improves after repeated use
67
What is the pattern of muscle weakness in myasthenia gravis?
Worsens with repeated use
68
What are the ocular symptoms in myasthenia gravis?
Drooping eyelids, diplopia
69
What are the bulbar symptoms in myasthenia gravis?
Facial weakness (myasthenic snarl), disturbed hypernasal speech, difficulty in smiling, chewing or swallowing
70
On examination of the eyes, what findings are present in myasthenia gravis?
Bilateral ptosis
Complex ophthalmoplegia
Test for ocular fatigue
71
What test is used to identify ptosis in myasthenia gravis?
Ice on eyes test
72
What is the ice on eyes test in myasthenia gravis?
Ice packs are placed on closed eyelids for 2 minutes, improving neuromuscular transmission, reducing ptosis.
73
What investigations are used to diagnose myasthenia gravis?
Serum acetylcholine receptor antibodies
MuSk antibodies
Tensilon test
Nerve conduction study - repetitive stimulation demonstrates decrements of the muscle action potential
74
What is the Tensilon test in myasthenia gravis?
Short-acting anti-cholinesterase (Edrophonium) increases acetylcholine levels by inhibiting acetylcholinesterase activity
Transient improvement in clinical features
75
What does a nerve conduction study reveal in myasthenia gravis?
Repetitive stimulation demonstrates decrements of the muscle action potential
76
What is the acute treatment of myasthenia gravis?
Intravenous immunoglobulin and plasma exchange (rapid immunosuppression)
77
What is the symptomatic treatment of myasthenia gravis?
Cholinesterase inhibitors (Pyridostigmine, neostigmine)
78
What are the side effects associated with cholinesterase inhibitors?
Risk of bradycardia and diarrhoea
Cholinergic crisis
79
What should be monitored and measured in myasthenia gravis?
Vital capacity to assess the risk of respiratory failure
80
Which immunosuppressants are recommended in myasthenia gravis?
Prednisolone
Azathioprine
Ciclosprin
81
What are the complications of myasthenia gravis?
Myasthenic crisis - respiratory failure, requiring intubation and mechanical ventilation
82
What is a subarachnoid haemorrhage?
An arterial haemorrhage in the subarachnoid space
| -Predominantly caused due to a rupture of saccular aneurysms at the base of the brain
83
Which vessels are predominantly implicated in a subarachnoid haemorrhage?
Circle of Willis
84
What are the risk factors for developing a subarachnoid haemorrhage?
Hypertension
Smoking
Excess alcohol intake
Polycystic kidney disease
Marfan's syndrome
Pseudoaxanthoma elasticum
Ehler's Danlos syndrome
85
What is the presentation of a subarachnoid haemorrhage?
Sudden onset severe headache in the occipital region
Thunderclap headache
-Nausea and vomiting
Neck stiffness
Photophobia
Decreased level of consciousness
Symptoms of meningism
Signs of raised intracranial pressure
86
What type of headache is associated with a subarachnoid haemorrhage?
Thunderclap headache, peaking within 1-5 minutes
87
What is the site of headache in a subarachnoid haemorrhage?
Occipital region
88
What is kernig's sign?
Pain on knee extension when the hip is flexed
89
What are the signs of raised intracranial pressure?
Papilloedema, IV or III cranial nerve palsies, hypertension and bradycardia
90
Why do focal neurological signs occur in a subarachnoid haemorrhage?
Develop on the second day and are caused by ischaemia from vasospasm and reduced brain perfusion
91
What is the main investigation for subarachnoid haemorrhage?
Emergency non-contrast CT scan
92
What does an emergency non-contrast CT scan reveal in a subarachnoid haemorrhage?
Hyperdense areas in basal regions of the skull (within the subarachnoid space)
93
What does a lumbar puncture reveal in a subarachnoid haemorrhage?
CSF opening pressure is increased
Red cells, xanthochromia
94
What is xanthochromia is a subarachnoid haemorrhage lumbar puncture?
Straw-coloured CSF due to breakdown of haemoglobin, confirm using spectrophotometry
95
What drug is prescribed in a subarachnoid haemorrhage?
Nimodipine
96
What role does nimodipine play in the management of a subarachnoid haemorrhage?
A calcium channel antagonist - reducing vasospasm
97
what is the surgical management for a subarachnoid haemorrhage?
Endovascular coiling (Platinum) of the aneurysm
Clipping or wrapping
98
What are the complications with a subarachnoid haemorrhage?
Obstructive hydrocephalus (CSF backflow within the ventricles)
99
What is a subdural haemorrhage?
A subdural haemorrhage is defined as an accumulation of blood between the dura and arachnoid layers of the brain
100
What defines an acute subdural haemorrhage?
Symptoms occurring within 72 hours
101
What defines a subacute subdural haemorrhage?
Symptoms within 3-20 days
102
What defines a chronic subdural haemorrhage?
After 3 weeks
103
What is the aetiology of a subdural haemorrhage?
Trauma- shear forces cause a disruption to the bridging cortical veins emptying into the dural venous sinuses
brain atrophy - Room for the haematoma to enlarge before causing symptoms
104
What is the presentation of a subdural haemorrhage?
History of trauma with head injury - patient has a decreased conscious level
Subacute - worsening headache 7-14 days after injury
Chronic
- Headache
- Confusion
- Cognitive impairment
- Psychiatric symptoms
- Gait deterioation
- Focal weakness (Aniscoria - unequal pupil size- sign of brainstem herniation)
- Seizures
- Diminished motor response
105
What are the examination findings in a subdural haemorrhage?
Decreased GCS
Anisocoria - Large haematomas result in a midline shift - ipsilateral fixed dilated pupil (Compression of the third nerve parasympathetic fibres)
Raised ICP - Decreased consciousness bradycardia, irregular breathing and widened pulse pressure
106
What is the definitive investigation for a subdural haemorrhage?
CT head
107
What is revealed in a CT head in a patient with a subdural haemorrhage?
Crescent-shaped, concave bleed over the brain surface.
Ct appearances change with time - acute haemorrhages --> Hyperdense
Become isodense over 1-3 weeks, effacement of sulci and midline shift, ventricular compression present
Chronic subdural - hypodense
108
What prophylactic anti-epileptics are administered in subdural haemorrhage?
Phenytoin or levetiracetam
109
How is coagulopathy corrected in subdural haemorrhage?
Reverse or stop anti-coagulant treatment
Correction involves administration of vitamin-K, FFP, platelets, cryptoprecipitate or protamine
110
What is the first-line management of a raised ICP?
Head elevation and consider osmotic diuresis with mannitol or hypertonic saline
111
What is the surgical management in symptomatic subdural haemorrhage?
Burr-hole or craniotomy and drainage
112
What is the Wernicke's Encephalopathy?
A neurological emergency resulting from a thiamine deficiency with varied neurocognitive manifestations.
• Changes in mental state status
• Gait and oculomotor dysfunction.
113
What is the aetiology of wernicke's?
Thiamine deficiency can occur because of reduced intake, increased demand, and malabsorption
114
What are the risk factors of Wernicke's?
* Alcohol dependence – Low storage capacity of the liver, decreased intestinal absorption and impaired thiamine metabolism.
* AIDs
* Cancer and treatment with chemotherapeutic agents
* Malnutrition
* History of gastrointestinal surgery – Bariatric surgery procedures for Class III obesity may predispose to thiamine malabsorption.
115
What is the presentation of Wernicke's?
* Cognitive dysfunction: Mental slowing, impaired concentration, and apathy.
* Frank confusion: Presenting manifestation in emergency departments and in patients who misuse alcohol.
* Ocular motor findings: Gaze palsies, sixth nerve palsies, and impaired vestibulo-ocular reflexes + Nystagmus, unequal pupils, nonreactive pupils.
* Mild irritability
* Delirium
* Acute psychosis
116
What are the triad of symptoms?
Ophthalmoplegia, ataxia, , and confusion
117
What are the investigations of Wernickes?
A therapeutic trial of parenteral thiamine – Clinical response to treatment.
N.B: Diagnosis is predominantly based on history and examination.
• FBC: High MCV is a common feature amongst alcoholics.
• U&Es: Exclude metabolic imbalances as a cause of confusion
• Glucose
• ABG: Hypercapnia and hypoxia can cause confusion.
118
What is the management of Wernicke's?
Stabilisation/resuscitation + thiamine + magnesium + multivitamins.
• Intravenous 250-500mg Thiamine
• Magnesium sulphate
• Multivitamin.
119
What is Korsakoff's psychosis?
• Korsakoff’s Psychosis: May present as profound anterograde amnesia with limited retrograde amnesia (Degeneration of mamillary bodies).
Confabulation – Fabrication of memories to mask memory deficit.
120
What is Meniere's disease?
Meniere's disease is an auditory disease characterised by an episodic sudden onset of vertigo, low-frequency roaring tinnitus and sensation of fullness in the affected ear.
121
What are endolymphatic hydrops?
• Endolymphatic hydrops Over-production or impaired absorption of endolymph – Excessive pressure causes distension and rupture of Reisner’s membrane.
122
What is the presentation of Meniere's disease?
* Vertigo – Recurrent episodes – spinning sensation lasting minutes – hours; usually associated with nausea and vomiting.
* Hearing loss- Fluctuating and worsens during or around the vertigo spells.
* Tinnitus- Unilateral in the affected ear.
* Aural fullness – May increase prior to an attack.
123
What is positive Romberg's sign?
Swaying or falling when asked to stand with feet together and eyes closed
124
What is Fukuda's stepping test?
Turning towards the affected side when asked to march in place with eyes closed.
125
What is tandem walk?
Inability to walk in a straight line (heel-toe)
126
What is the first-line investigation for Meniere's disease?
Pure-tone audiometry
Air-bone conduction is equal- indicates the underlying pathology is in the cochlear or the auditor nerve
Unilateral sensorineural hearing loss - Inner ear is affected - low frequency
127
What are otoacoustic emissions?
The measure of outer hair cell dysfunction: Absence of measurable OAE in frequency range affected by MD.
128
What is the management of MD?
Dietary changes and lifestyle modification: Restrict salt intake (prevent-sodium related water retention and redistribution into the endolymphatic system).
• Limit caffeine intake, reduce alcohol consumption, smoking cessation and stress management to minimise triggers.
Diuretic: For symptomatic vertigo.
Vestibular suppressant, anti-emetic, or corticosteroid
• Antihistamines (Meclozine, dimenhydrinate, promethazine)
• Benzodiazepines (Diazepam and phenothiazines) – Used in acute attacks only.
• Oral corticosteroids: Used to treat acute attacks of vertigo, especially when accompanied by acute hearing loss and tinnitus.
Persistent hearing loss: Hearing aid or assistive listening device.
Surgical (Failure of therapies): Endolymphatic sac surgery.
129
What is the definition of a stroke?
A stroke is a rapidly developing focal disturbance of brain function due to cerebrovascular insult lasting >24 hours.
Can be subdivided based on:
• Location: Anterior v Posterior circulation
• Pathological process: Infarction v haemorrhage.
130
what is the most common type of stroke?
Ischaemic stroke
131
What is the common cause of embolic stroke?
Carotid dissection, carotid atherosclerosis, atrial fibrillation
Venous blood clots
132
What is the presentation of a stroke?
Stroke affects 5 core functions: Motor, sensation, speech, balance, and vision.
• Sudden onset (Deterioration within seconds).
• Weakness
• Sensory, visual, or cognitive impairment
• Impaired coordination
• Impaired consciousness
• Head or neck pain (If carotid or vertebral artery dissection).
133
What are the symptoms of an ACA stroke?
* Hemiparesis – Contralateral lower limb weakness (Topographic organisation of the primary motor cortex).
* Confusion
* Abulia: Disturbance of intellect, executive function, and judgement.
* Loss of appropriate social behaviour (Disinhibition)
134
What are the symptoms of an MCA stroke?
The MCA primarily supplies a portion of the frontal lobe and the lateral surface of the temporal and parietal lobes.
• Contralateral hemiplegia – Topographically affecting the upper limb + Facial weakness.
• Contralateral hemisensory deficits – Primary somatosensory cortex is affected.
• Hemineglect
• Hemianopia
• Apraxia
• Aphasia (In a left-sided lesion) Broca’s and Wernicke’s area is affected.
• Quadrantanopia (If superior or inferior optic radiations are affected).
135
What are the symptoms of a PCA stroke?
The PCA is largely responsible for supplying the occipital lobe, in addition to the inferior region of the temporal lobe.
• Homonymous hemianopia (one side) and visual agnosia (Inability to recognise objects).
• Prosopagnosia – A cognitive disorder of facial recognition.
136
What are the symptoms of an anterior-inferior cerebellar stroke?
Vertigo, ipsilateral ataxia, ipsilateral deafness, ipsilateral facial weakness
137
What are the symptoms of a posterior inferior cerebellar stroke?
```
Vertigo
Ipsilateral ataxia
Ipsilateral Horner's syndrome
Ipsilateral hemisensory loss
Dysarthria
Contralateral spinothalamic sensory loss
```
138
What are lacunar infarcts?
Affecting the internal capsule or pons (pure sensory or motor deficit)
Affecting the thalamus or the basal ganglia.
139
What are the investigations for a stroke?
```
Urgent non-contrast CT
Blood glucose
U&Es
Clotting screen
ECG
Echocardiogram
Carotid Doppler Ultrasound
```
140
What is the management of a hyperacute stroke <4.5 hours?
Intravenous thrombolysis
Alteplase (IV tPA)
Do not administer aspirin within the first 24 hours of presentation
141
What is the management of an acute ischaemic stroke beyond 4.5 hours?
2 weeks of 300mg Asipirin and 75mg lifelong clopidogrel
142
What is the surgical management for a stroke?
Carotid endarterectomy within 2 weeks of stroke
143
What is a TIA?
Rapidly developing focal disturbance of brain function of presumed vascular origin that resolves completely within 24 hours.
144
What is the most common cause of a TIA?
Embolic causes - carotid atherosclerosis
145
What is the first-line management of a TIA?
300mg aspirin
146
How long do TIAs typically last?
10-15 minutes
147
What are the global events that occur in a TIA?
Syncope and dizziness (typical of ECG)
148
What is amaurosis fugax?
Painless fleeting loss of vision caused by retinal ischaemia
149
What investigations are performed in a patient presenting with a TIA?
300mg Aspirin
Clopidogrel 300mg then 75mg thereafter
Atorvastatin 20-80mg
150
What are the indications for performing a carotid endarcetectomy?
>70% stenosis at the origin of the ICA
151
What is the definition of a migraine?
A migraine is defined as a severe episodic headache that is associated with a prodrome of focal neurological symptoms and systemic disturbance.
152
What are classic migraines?
Migraines with an aura
153
What are the typical prodromal symptoms in a migraine?
```
Changes in mood
Urination
Fluid retention
Food craving
Yawning
Aura
```
154
What are auras in migraines?
Visual disturbances can develop
Sensory disturbances (numbness, paraesthesia)
Positive symptoms: Scintilating scotomas - zig-zag crescent
Negative symptoms: Blind spots and visual occlusions
155
Describe a migraine headache?
Pulsating hemicranial nausea and photophobia with headache
156
What is the typical duration of a migraine?
3-12 hours
157
What are the triggers of a migraine?
: Stress, exercise, lack of sleep, oral contraceptive pill, food (caffeine, alcohol, cheese, chocolate), and pattern of analgesic use.
158
What is the first-line management of a migraine?
Tiprants - Sumatripain
NSAIDs
Metoclopramide
159
What is the prophylactic treatment of a migraine?
Beta-blockers (Propranolol)
| Topiramate (Contraindicated in asthma)
160
What are tension headaches?
Generalised throughout the head, with a predilection involving the frontal and occipital regions
161
How does a tension headache feel?
Tight band around the head
162
How often do episodic Tension headaches occur?
<15 days per month
163
Which sex experiences tension headaches more?
Women
164
What is the presentation of a tension headache?
A generalised headache that is moderate in severity
• Pressure around the head (Tight band).
• Non-pulsatile, bilateral pain.
• Often a relationship with the neck
• Can be disabling for a few hours but does not have specific associated symptoms.
• Gradual onset
• Variable duration
• Usually responsive to over-the-counter medication.
165
What is the management of a tension headache?
* Reassurance
* Address triggers (Stress, anxiety)
* Advice on avoiding medications that can cause medication-induced headaches (opioids).
* Simple analgesia (Ibuprofen, paracetamol, aspirin)
* Tricyclic antidepressants may be considered in frequency recurrent episodic tension headaches or chronic tension headaches.
166
Define trigeminal neuralgia?
Trigeminal neuralgia (TN) is a facial pain syndrome in the distribution of the trigeminal nerve divisions, characterised by a paroxysm of sharp, stabbing, intense pain lasting up to 2 minutes
167
What is the most common aetiology of trigeminal neuralgia?
Compression of the trigeminal nerve root at the root entry zone by an aberrant vascular loop (Mainly the superior cerebellar artery).
168
What is the presentation of trigeminal neuralgia?
Sudden, unilateral, brief, stabbing pain in the distribution of one or more of the branches of the trigeminal nerve.
169
How long does the pain last for trigeminal neuralgia?
Few seconds to a couple of minutes
170
How is the pain described in trigeminal neuralgia?
Shock-like pain
171
What are the triggers of trigeminal neuralgia?
```
Vibration
Skin contact- washing, shaving
Eating
Dental prostheses
Brushing teeth
Exposure to wind
```
172
What investigations are performed in trigeminal neuralgia?
Note: Diagnosis is predominantly based on clinical presentation
Consider performing an MRI to visualise abnormal vessel loop in association with the trigeminal nerve.
173
What is the first-line therapy for trigeminal neuralgia?
Anti-convulsant - Carbamazepine
Baclofen - if unresponsive to anti-convulsant treatment
174
What is Guillain Barre Syndrome?
An acute inflammatory neuropathy characterised by motor difficulty, absence o tendon reflexes and paraesthesia
Antibodies following a recent infection react with self-antigen on myelin on neurones
175
What is the pattern of motor difficulty in GBS?
Progressive symptoms of muscle weakness, initially affecting the lower extremities
176
Presentation of GBS
* Muscle weakness – usually affecting the lower extremities before upper extremities and proximal muscles.
* Paraesthesia- In hands and feet, preceding the onset of weakness.
* Back/leg pain – May precede muscle weakness.
* Respiratory distress – Include dyspnoea on exertion and shortness of breath.
* Speech problems – Facial weakness and slurred speech
* Areflexia/hyporeflexia
* Facial weakness
* Bulbar dysfunction
* Extra-ocular muscle weakness
* Facial droop
* Diplopia
* Dysarthria
* Dysphagia
* Dysautonomia
177
On examination what are the features of GBS?
Hypotonia
Flaccid paralysis
Areflexia
178
What triad is associated with Miller-Fischer Synrome?
Ataxia
Areflexia
Opthalmoplegia
179
What are the investigations in GBS?
Nerve conduction studies
Lumbar puncture
Blood
Spirometer
180
What is spirometry performed in GBS?
Reduced vital capacity and maximal inspiratory/expiratory pressures - indicating type 2 respiratory failure due to paralysis of respiratory muscles
181
What would a lumbar puncture reveal in GBS?
Elevated CSF protein
182
What antibodies are associated with Miller-Fischer Variant of GBS?
Anti-ganglioside antibodies
183
What is the first-line management of GBS?
Intravenous immunoglobulin
| Plasma exchange with IVIG
184
Define epilepsy
A recurrent tendency to spontaneous, intermittent, abnormal electrical activity in the part of the brain, manifesting as seizures (paroxysmal synchronised cortical electrical discharge).
• > 2 seizures for epilepsy to be diagnosed.
185
What are the two main categories of seizures?
Partial
| Generalised
186
What are the two types of partial seizures?
Complex
| Simple
187
What are partial seizures?
Focal onset seizure localised to specific cortical regions
188
What is a complex partial seizure?
Consciousness is affected
189
What is a simple partial seizure?
Consciousness is not affected
190
What is a generalised seizure?
Seizures that affect the whole of the brain - also affects consciousness
191
What are the four types of seizures?
Tonic-clonic
Absence
Myoclonic
Atonic
192
What are tonic-clonic seizures?
Limbs stiffen (tonic) then jerk (clonic)
193
What are absence seizures?
Brief pauses
194
What are myoclonic seizures?
Sudden jerk of a limb, face or trunk
195
What are atonic seizures?
Sudden loss of muscle tone causing fall
196
What is the presentation of a frontal motor seizure?
```
Motor convulsions
Jacksonian March (Muscular spasm caused by simple partial seizure spreads from affecting the distal part of the limb towards the ipsilateral face)
```
Post-ictal flaccid weakness (Todd's paralysis)
197
What is a Jacksonian March?
Muscular spasms caused by simple partial seizures spread from affecting the distal part of the limb towards the ipsilateral face
198
What is the presentation of a temporal lobe seizure?
Aura - visceral or psychic symptoms
Hallucinations (Olfactory or affecting taste)
199
Olfactory hallucinations are associated with which type of seizure?
Temporal lobe seizures
200
Lip-smacking is associated with which type of seizure?
Temporal lobe seizures
201
What lobe specific symptoms are associated with a parietal lobe seizure?
Sensory -Paraesthesia
202
What is the presentation of a tonic-clonic seizure?
Tonic phase - generalised muscle spasms
Clonic phase - Repetitive synchronous jerks
Faecal/urinary incontinence
Tongue biting
203
What is associated in the post-ictal phase of a tonic-clonic seizure?
Impaired consciousness, lethargy, confusion, headache back pain and stiffness
204
What is the presentation of an absence seizure?
* Onset in childhood
* Loss of consciousness but maintained posture
* The patient will appear to stop talking and stare into space for a few seconds
* No post-ictal phase.
205
What investigation is used to confirm the diagnosis of epilepsy?
EEG
206
What is status epilepticus?
A seizure lasting >30 minutes or repeated seizures without recovery and regain consciousness in between
207
What is the first-line management of status epilepticus?
IV lorazepam or IV/pr diazepam - repeat again after 10 minutes
208
If seizures recur despite lorazepam management, what management should be considered?
IV phenytoin
209
What is the first-line therapy for generalised seizures?
Sodium valproate
Lamotrigine
Ethosuximide
210
What is the first-line therapy for partial seizurs?
Carbamazepine
211
Which anti-epileptic drug should be used in women of child-bearing age?
lamotrigine
| And folic acid
212
What are the complications of lamtorigine?
Steven-Johnson Syndrome
213
What are the complications of carbamazepine?
Neutropenia and osteoporosis
214
What is BPPV?
BPPV is a peripheral vestibular disorder (labyrinth and/or vestibulocochlear nerve) that manifests as sudden, short-lived episodes of vertigo elicited by specific head movements.
215
what is the average duration of a BPPV episode?
30 seconds
216
What is the average age of onset of BPPV?
55 Years
217
What is the pathophysiology of BPPV?
Otoliths from the utricle are detached from the maculae and are dislodged into the semi-circular canals.
• Otoliths stimulate a larger endolymph flow when the head is in motion, thus facilitating the movement of the head will be processed by the brain as bigger and faster than perceived.
• Settle into the posterior semi-circular canal – Most gravity-dependent regions of the vestibular labyrinth.
• The posterior semi-circular canal has an impermeable barrier that enables otolith particles to be trapped as opposed to the lateral and anterior semi-circular canal.
218
What repositioning manoeuvres are associated with improving vertigo in BPPV?
Epley
| Sermont
219
Which semi-circular canal is most affected in BPPV?
Posterior semi-circular canal
220
What is the presentation of BPPV?
Brief duration of vertigo <30 seconds
Associated symptoms : Nausea, imbalance, and light-headedness
Episodic vertigo
221
What are the associated symptoms with BPPV?
Nausea, imbalance and light-headedness
222
Which manoeuvre can be used to diagnose BPPV?
Hallpike
- Positive supine lateral head turn
- Rotatory nystagmus
223
What is the management for BPPV?
Epley Manoeuvre
• Teaching the patient exercises they can do themselves at home, termed vestibular rehabilitation for example Brandt-Daroff exercises.
N.B: Good prognosis – Resolves spontaneously within a few weeks to months.
224
What is epistaxis categorised into?
Posterior and anterior bleeds
225
Which plexus is associated with anterior nose bleeds?
Kiesselbach's plexus
226
Where do the majority of nose bleeds occur?
Little's area of the anterior septum
227
What are the causes of secondary epistaxis?
* Alcohol
* Antiplatelet drugs (Clopidogrel)
* Aspirin and NSAIDs
* Anticoagulants (Warfarin)
* Coagulopathy (Haemophilia, von Willebrand’s disease)
* Trauma (Nasal fracture)
* Tumours
* Surgery
* Septal perforation
* Cocaine use – Septum may look abraded or atrophied – inquire about drug use. Cocaine is a potent vasoconstrictor and repeated use can cause obliteration of the septum.
* Juvenile angiofibroma – Benign tumour that is highly vascularized (Seen in adolescent males).
* Hereditary haemorrhagic telangiectasia
228
What is the presentation of epistaxis?
Blood at one nostril or on both sides of the nose
Septal deviation
Recurrent epistaxis - common in children
Bleeding starting at the nares - anterior bleed causes blood in the pharynx
229
What is the first-line management of nose bleeds?
Inform the patient to sit with their torso forward and mouth open (Avoid lying down)
Decreases blood flow to the nasopharynx and allows the patient to spit out any blood
pinch the soft area of the nose firmly for a minimum of 20 minutes
230
How long should the nose be pinched for in an acute nosebleed?
20 minutes
231
What treatment is available in recurrent nose bleeds?
Nasal cautery
Silver nitrate sticks
Nasal packing
232
What is the definition of tonsillitis?
Refers to the intense acute inflammation of the tonsils - an infection of the parenchyma of the palatine tonsils
Associated with a purulent exudate
233
What is the predominant causative organism in tonsilitis?
Streptococcus pneumoniae
234
What is bacterial tonsilitis associated with?
Cervical lymphadenopathy
235
What symptoms are associated with viral tonsilitis?
Associated with headache, apathy and abdominal pain
236
What is the CENTOR criteria?
Gives an indication of the likelihood of a sore throat being due to a bacterial infection
1. Tonsillar exudate
2. Tender anterior cervical lymphandenopathy
3. Fever over 38
4. Absence of cough
237
What is the presentation of tonsilitis?
* Pain on swallowing
* Fever >38
* Tonsillar exudate
* Sudden onset sore throat
* Headache
* Nausea and vomiting
* Tonsillar erythema and enlargement
238
What investigations are performed in bacterial tonsilitis?
Throat culture
| Rapid streptococcal antigen test
239
What is the first-line management for bacterial tonsitilitis?
Penicillin V 500 mg PO QDS for 5-10 days
240
What are the indications for a tonsillectomy?
If a patient suffers more than 5 episodes of tonsillitis per year for 2 years and interferes with daily life Refer for tonsillectomy.
241
Define Rhino-sinusitis
Acute sinusitis is a symptomatic inflammation of the mucosal lining of the nasal cavity and paranasal sinuses – Presenting with purulent nasal drainage accompanied by nasal obstruction, and facial pain <4 weeks.
242
What are the two key features of rhino-sinusitis?
Nasal congestion
| Nasal discharge
243
What are the predisposing factors for rhinosinusitis?
Nasal obstruction - Septal deviation or nasal polyps
Recent local infection: Rhinitis or dental extraction
Swimming/diving
Smoking
244
What are the predominant causative infectious organisms in rhinosinusitis?
Streptococcus pneumoniae, Haemophilus influenzae and rhinovirus.
245
What is the presentation of rhinosinusitis?
Purulent nasal discharge
Nasal obstruction
Facial pain/pressure - Frontal Pain which is worse on bending forward
246
What is the management for rhinosinusitis?
Conservative management
• Analgesia
• Intranasal corticosteroids if symptoms persist > 10 days.
• Intranasal decongestants or nasal saline
```
Severe presentations (Antibiotics)
• Phenoxymethylpenicillin first-line
```
247
What is obstructive sleep apnoea?
OSA is characterised by episodes of complete or partial upper airway obstruction during sleep
248
What are the predisposing factors of OSA?
Obesity
Macroglossia - Acromegaly, hypothyroidism, amyloidosis
```
Large tonsils
Marfan's syndrome
Micrognathia
Neuromuscular disease
Alcohol
```
249
What is the presentation of OSA?
```
Excessive daytime sleepiness
Lack of concentration
Chronic snoring
Restless sleep
Insomnia
Irritability/personality change
Episodic gasping
```
250
What investigations are performed in OSA?
Polysomnography
251
How many episodes/hour on the Apnoea-Hypopnea diagnose for OSA?
>15 episodes
252
How is sleepiness assessed?
Epworth Sleepiness Scale
253
What is the first-line management of OSA?
Continuous positive airway pressure (CPAP)
254
What are the complications of OSA?
* Impaired glucose metabolism
* Cardiovascular disease
* Depression
* Motor vehicle accidents
* Cognitive dysfunction
* Increased mortality
255
What is Parkinson's Disease?
A neurodegenerative disorder of the dopaminergic neurones of the Substantia nigra.
256
Which part of the brain is affected in Parkinson's disease?
Substantia Nigra
257
What is the pattern of symptoms presented in Parkinson's disease?
Asymmetrical
258
What is the triad of symptoms in Parkinson's disease?
Bradykinesia
Rigidity
Resting tremor
259
What is bradykinesia?
Slowness of small movements
260
What tremor is associated with Parkinson's disease?
Pill-rolling tremor starting in one hand.
261
Which neurones are affected in PD?
Dopaminergic neurones
262
What is drug-induced PD?
Concerns a rapid onset and bilateral character of symptoms
| Rigidity and rest tremor are uncommon
263
Which drugs can induce PD?
Anti-psychotics
| Anti-emetics - Metoclopramide
264
What is the onset of PD?
Insidious
265
What frequency is the pill-rolling resting tremor in PD?
3-5 Hz
266
When is the pill-rolling tremor most marked?
At rest
267
When is the pill-rolling tremor worse?
When stressed or tired, improves with involuntary movement
268
What kind of rigidity is associated with PD?
lead pipe
| Cogwheel
269
What are the symptoms of PD?
```
• Insidious Onset
• Resting tremor (Mainly in hands) – Asymmetrical
- Most marked at rest, 3-5 Hz
- Worse when stressed or tired – Improves with voluntary movement
- Pill-rolling – Thumb and index finger
• Bradykinesia
- Stiffness and slowness of movements
- Poverty of movement (Hypokinesia)
- Akinesia: Difficulty initiating movements
• Rigidity
- Lead pipe
- Cogwheel: Due to superimposed tremor
- Enhanced by distraction
• Frequent falls
• Micrographic – Smaller handwriting
• Insomnia
• Mental slowness (Bradyphemia)
• Subtle: Sense of smell reduced, constipation, visual hallucinations, frequency/urgency, dribbling of saliva, depression.
```
270
What face is seen in a patient with PD?
Hypomimic face - Expressionless, mask-like
271
What gait is seen in PD?
Shuffling gait
272
What are the investigations for PD?
Diagnosis is confirmed based on history and examination
Levodopa trial --> Improvement in symptoms (Indicated in patients presenting with atypical features)
273
What investigation is performed to differentiate between essential tremor and Parkinson's disease?
I-FP-CIT single proton emission computed tomography (SPECT)
274
What is the first-line management for Parkinson's disease?
Levodopa (If motor symptoms are affecting quality of life)
275
If motor functions are not affecting the patient's quality of life in PD, what drug can be adminsitered?
Oral monoamine oxidase-B inhibitors
-• Selegiline, rasagiline or safinamide
276
What are the common complications of PD medication?
Acute akinesia, neuroleptic malignant syndrome
277
What is encephalitis?
Inflammation of the brain parenchyma associated with neurological dysfunction
278
What are the initial symptoms of encephalitis?
Pyrexia and headache
279
What is the most common viral cause of encephalitis?
HSV
280
What is the presentation of encephalitis?
* Fever
* Seizures
* Vomiting
* Headache
* Behavioural changes/Mental state alteration – Confusion
* History of seizures
* Focal neurological symptoms: Dysphagia, hemiplegia, aphasia (Hallmark feature)
Signs of meningism- neck stifness and photophobia
281
What are the hallmark features of encephalitis?
Focal neurological symptoms: Dysphagia, hemiplegia, aphasia
Behavioural changes/Mental stage alteration
282
What examination findings are evident in encephalitis?
Reduced consciousness, deteriorating GCS
```
Seizures
Pyrexia
Neck stiffness
Photophobia
Kernig test positive
```
Signs of Raised ICP - Cushing's Triad
Vesicular eruption
283
What investigations are performed in encephalitis?
CSF - lymphocytosis and elevated protein
MRI/CT
FBC
Lumbar puncture
284
What does a Lumbar puncture reveal in encephalitis?
```
High lymphocytes
High monocytes
High protein
Normal or low glucose
Viral PCR - 95% specific for HSV-1
```
285
Which part of the brain is affected by HSV encephalitis?
Temporal lobe
286
What is the first-line management of encephlalitis?
Intravenous acyclovir
287
What is a brain abscess?
Suppurative collection of microbes within a gliotic capsule occurring within the brain parenchyma
288
What are the risk factors of a brain abscess?
* Sinusitis
* Otitis media
* Recent dental procedure or infection
* Recent neurosurgery
* Meningitis
* Congenital heart disease
* Endocarditis
* Diverticular disease
* Hereditary haemorrhage telangiectasia
* HIV
289
What is the presentation of a brain abscess?
* Meningismus
* Headache- Often dull, persistent.
* Cranial nerve palsy- Third or sixth palsies, anisocoria, and papilledema (Secondary to raised ICP).
* Positive Kernig or Brudzinski sign
* Fever
* Neurological deficit
* Infants: Bulging fontanelles, and increased head circumference
290
What investigations are performed in a brain abscess?
CT scan - ring-enhancing lesions
FBC -leukocytosis
291
What is the management of a brain abscess?
A craniotomy is performed, and the abscess cavity is debrided
IV antibiotics - Cephalosporin + metronidazole
292
What drug can be used to manage intracranial pressure in a brain abscess?
Dexamethasone
293
What is carpal tunnel syndrome?
Compression of the median nerve in the carpal tunnel
294
Which nerve is affected in carpal tunnel syndrome?
Median nerve
295
What is the aetiology of carpal tunnel syndrome
Repetitive stress injury in susceptible people Inflammation Oedema Fluid in narrow space compresses structures Nerve injury.
296
What are the causes of carpal tunnel syndrome?
Tendonitis
Oedema
Repetitive stress injury
297
What are the risk factors for carpal tunnel syndrome?
* Obesity
* Pregnancy
* Underlying conditions (Rheumatoid arthritis)
* Trauma
* Genetic predisposition
* Occupation
298
What is the presentation of carpal tunnel syndrome?
* Numbness of hands – Dominant hand is usually affected (Fingers affected: Thumb, index, middle finger).
* Night-time worsening – Waking up at night with paraesthesia/pain in hand/wrist and shaking the hand to relieve symptoms.
* Symptoms are intermittent
* Gradual onset
* Weakness of hand
* Clumsiness
* Aching and pain in the arm
299
Which three fingers are affected in Carpal tunnel syndrome?
Thumb, index and middle finger
300
When are the symptoms of carpal tunnel syndrome worse?
During the night
301
What is Tinel's sign in carpal tunnel syndrome?
Tapping causes paraesthesia
302
What is Phalen's Sign in carpal tunnel syndrome?
Flexion of the wrist causes symptoms (Pressing of upper hands together when flexing wrists induces pain)
303
What is the treatment of carpal tunnel syndrome?
Corticosteroid injections to decrease inflammation
Wrist splints at night
Surgical decompression
304
Define Erb Palsy?
A brachial plexus birth palsy, encountered because of a delivery complicated by shoulder dystocia
305
Which nerve roots are involved in Erb Palsy?
C5 and C6
306
Which peripheral nerves are affected in erb palsy?
Axillary
Musculocutaneous
Suprascapular
307
What is neuropraxia in Erb Palsy?
A stretch injury of the axon that does not cause division of the neural tissue
- Conduction block
- Resolves quickly
308
What is the presentation of Erb palsy?
Paralysis of an arm - Lack of movement. of an affected extremity
Decreased motion of an arm
The abnormal posture of the arm
309
What investigations are performed in Erb Palsy?
X-ray of chest and affected upper extremity
Ultrasound scan of the shoulder to detect dislocation
310
What is the treatment of Erb Palsy?
Physiotherapy
Surgical nerve repair/reconstruction
311
What is Klumpke Paralysis?
a type of brachial plexus affecting the lower brachial plexus nerve roots c8-T1
312
Which nerve roots are affected in Klumpke paralysis?
C8-T1
313
What is the presentation of Klumpke Paralysis?
Claw hand
Intrinsic hand muscle atrophy
Sensation loss in the medial side of the upper arm, upper arm weakness
Horner syndrome
314
What is Horner's syndrome?
Ptosis (Drooping eyelid)
Enopthalmos (Deep set eye)
Miosis (Constricted pupil)
Anhidrosis
315
What is Alzheimer's Dementia?
Alzheimer’s dementia is a chronic neurodegenerative disease with progressive and (Slow cognitive decline) and an insidious onset.
• Most common type of dementia (60-70%)
• Characterised by memory impairment.
316
Which extracellular protein is associated with AD?
Amyloid precursor protein
317
Which intracellular protein is associated with AD?
Neurofibrillary tangles -Tau proteins
318
Which part of the brain is affected predominantly in AD?
Hippocampus, amygdala, basalis of Meynert
AcH deficiency
319
Which neurotransmitter is deficient in AD?
Acetylcholine
320
What are the symptoms of AD?
* Amnesia – Loss of short-term memory
* Anomia – Inability to name objects
* Apraxia – Loss of dexterity
* Agnosia – Inability to recognise things, unable to understand the function of objects
* Aphasia – inability to talk
* Decline in ADLs
* Personality change – Exaggeration of premorbid traits with coarsening of affect and egocentricity.
* Behavioural disturbances: Aggression, wandering, explosive temper, sexual disinhibition, incontinence, excessive eating, and searching behaviour.
321
What investigations are performed in suspected AD?
```
Mini-Mental State Examination (MMSE)
• Impaired recall
• Dysphagia
• Disorientation
• Impaired executive functioning
```
Metabolic panel
• Exclude abnormal sodium calcium and glucose
• TFTs
MRI
• Generalised atrophy with medial temporal lobe and later parietal lobe
322
What does an MRI suggest? in a patient with AD?
• Generalised atrophy with medial temporal lobe and later parietal lobe
323
What is the first-line treatment of AD?
Acetylcholinesterase inhibitors
| Donepezil
324
What is the mechanism of action of Donepezil, galantamine, and rivastigmine?
Acetylcholinesterase inhibitors
325
What is the mechanism of action of memantine?
NMDA receptor antagonist
326
What is vascular demntia?
Vascular dementia is associated with reduced blood supply to the brain due to diseased vessels and multiple infarcts within the minor blood vessels of the brain – Associated with cardiovascular disorders.
The executive functions of the brain affected more > memory – Underlying damages to both grey and white matter.
327
What type of progression is seen in vascular dementia?
Stepwise progression
328
What are the risk factors for vascular dementia?
Age > 60 years
Obesity
Hypertension
Cigarette smoking
329
What is the presentation of vascular dementia?
Cognitive-executive decline - Increased time to process information and formulate thoughts and structured communication
Personality changes - low mood, emotionally sensitive, or less environmentally withdrawn
-Frontal cognitive syndrome - apathy
Motility - Difficulty in walking/stability/gait
330
What is the management for vascular dementia?
Antiplatelet therapy + lifestyle modification
Aspirin
Cholinesterase inhibitor
Statin therapy
Carotid endarterectomy
331
What is Lewy-body dementia?
Defined as progressive cognitive decline - interfering with ADLs and is characterised by three of the following:
Fluctuating cognition
Recurrent visual hallucinations
REM sleep behavioural disorder
332
What are the triad of symptoms associated with Lewy-Body dementia?
1. Fluctuating cognition
2. Recurrent visual hallucinations
3. REM sleep behaviour disorder
333
What other features are associated with Lewy-Body dementia?
Parkinsonism
Bradykinesia
Rest tremor or rigidity
334
What is the aetiology of Lewy-body dementia?
Is associated with aberrant deposits of alpha-synuclein protein with the brain - predominantly within the primary motor cortex
335
Which part of the brain is predominantly affected in LB dementia?
Primary motor cortex
336
Which deposits are associated with LB dementia?
Alpha-synuclein protein
337
What is the presentation of LB dementia?
• Cognitive fluctuations
- Cognition
- Attention
- Arousal
• Visual hallucinations
- Well formed
* Motor symptoms
* REM sleep behavioural disturbance
338
What is the first-line management for LB dementia?
Cholinesterase inhibitors (Donepezil)
339
What is frontotemporal dementia?
Associated with neuronal atrophy of the frontal and temporal lobes due to the presence of abnormal proteins within them – Phosphorylated tau orTDP-43.
• Appear in mid-life with average age of onset between 45-65 years.
340
What are the symptoms of front-temporal dementia?
```
Symptoms
• Coarsening of personality, social behaviour and habits
- Slovenly appearance
- Impatience
- Irritability
- Argumentativeness
- Impulsiveness
```
* Progressive loss of language fluency or comprehension
* Development of memory impairment, disorientation, or apraxia
* Progressive self-neglect
341
What is meningitis?
Refers to the inflammation of the meninges (dura mater, arachnoid mater and pia mater)
342
What are the common bacterial causes of meningitis?
* Streptococcus pneumoniae (pneumococcus)
* Neisseria meningitides (meningococcus)
* Haemophilus influenzae
* Listeria monocytogenes
343
What is the presentation of meningitis?
* Headache
* Fever
* Neck stiffness
* Photophobia
* Nausea and vomiting
* Focal neurology
* Seizures
* Reduced conscious level
* Features of sepsis (non-blanching petechial rash of impending DIC)
344
What is Kernig;s sign?
Pain in the lower back or back of the thigh on the extension of the knee when the hip is flexed to a right angle.
345
What is Brudzinkski's sign?
Forced flexion of the neck elicits a reflex flexion of the hips
346
What investigations should be performed in meningitis?
Blood cultures within 1 hour of arrival at the hospital and prior to administering antibiotics.
Serum pneumococcal and meningococcal PCR
FBC
• Leucocytosis, anaemia, and thrombocytopenia
Serum urea, creatinine, and electrolytes
• In severe bacterial meningitis – metabolic acidosis, hypokalaemia, hypocalcaemia, and hypomagnesemia.
Cerebrospinal fluid (Lumbar puncture)
347
What is the first-line management of meningitis?
IM benzylpenicillin and urgent hospital transfer
348
What is raised intracranial pressure?
The brain and ventricles are enclosed by a rigid skull having a limited ability to accommodate additional volume.
• Additional volume: Haematoma, tumour, excessive CSF – Lead to a rise in intracranial pressure.
349
What are the causes of raised ICP?
* Idiopathic intracranial hypertension
* Traumatic head injuries
* Infection: Meningitis
* Tumours
* Hydrocephalus
350
What is the presentation of raised ICP?
* Headache
* Vomiting
* Reduced levels of consciousness
* Papilledema
Cushing’s triad
• Widening pulse pressure
• Bradycardia
• Irregular breathing
351
What is Cushing's triad?
Widening pulse pressure
Bradycardia
Irregular breathing
352
How is ICP monitored?
A catheter is placed into the lateral ventricle of the brain to monitor the pressure
353
What neuroimaging is performed in raised ICP?
CT/MRI
354
What is the management of raised ICP?
Head elevation to 30 degrees
IV mannitol or hypertonic saline
Controlled hyperventilation
Removal of CSF
355
What is essential tremor?
Essential tremor is a symmetrical and rhythmic involuntary oscillation movement disorder of the hands and forearms.
• Absent at rest
• Present during posture and intentional movements
356
What is the pattern of tremor in essential tremor?
Symmetrical
| Absent at rest
357
When is an essential tremor evident?
* Postural or kinetic (A postural tremor occurs when you attempt to hold parts of your body still against gravity).
* Tremor amplitude increases with time
* Patients have trouble with writing, eating, holding objects, and doing fine motor tasks.
358
What is the first-line management of essential tremor?
Propanolol
359
What investigations are performed in radiculopathy?
Spinal X-ray - narrowing of vertebral openings or disc injury
CT scan to visualise spinal cord
Nerve conduction studies
360
What is temporal arteritis?
Temporal arteritis is a large vessel vasculitis that overlaps with polymyalgia rheumatica (PMR), predominantly affecting branches of the external carotid artery.
• Occurs in people aged >50 years and is more common in women.
361
What is often coexistent with temporal arteritis?
Polymylagia rheuamtica
362
Which artery is predominantly affected in temporal arteritis?
Branches of the external carotid artery
363
What are the symptoms of temporal arteritis?
• Headache
- Associated with scalp tenderness (Noticed when brushing hair)
• Aching and stiffness
- Aching and stiffness in the neck, shoulders, hip, and proximal extremities that worsens after a period of inactivity and with movement.
- Symptoms of polymyalgia rheumatica
• Limb claudication
• Loss of vision
- Amaurosis fugax: Transient monocular blindness, described as a dark curtain descending vertically.
- Blurring
- Double vision
• Jaw and tongue claudication
• Arterial tenderness, thickening or nodularity
• Absent pulse
• Abnormal fundoscopy
364
What is the pattern of stiffness in temporal arteritis?
Neck, shoulder, hip and proximal extremities that worsens after a period of inactivity and with movement
365
What visual impairments are associated with temporal arteritis?
Amaurosis fugax
Blurring
Double vision
366
What is Amaurosis fugax?
Transient monocular blindness, described as a dark curtain
367
Which inflammatory markers is raised in temporal arteritis?
ESR >50 mm/hr
368
What is the definitive diagnostic investigation in temporal arteritis?
Temporal artery biopsy
| -Skip lesions in the artery
369
What is the first-line treatment in temporal arteritis?
Prednisolone high dose 60 mg OD
Bisphosphonates and PPIs to reduce osteoporosis and gastric ulcer risk
370
What should be administered in temporal arteritis if there is visual loss?
Methylprednisolone
371
What is an extradural haemorrhage?
A collection of blood that resides between the skull and dura, predominantly caused by trauma
372
Which artery is predominantly affected in an extradural haemorrhage?
Middle meningeal artery
373
Which part of the skull is susceptible to fracture?
Pterion
374
What is the initial presentation of an extradural haemorrhage?
Brief loss of consciousness followed by a lucid interval
Deterioration of consciousness and headache
Fixed and dilated pupil due to compression of the third cranial nerve
375
What is the lucid interval in an extradural haemorrhage
• Brief loss of consciousness, followed by regaining of normal consciousness level (Lucid interval).
The lucid interval is lost eventually due to the expanding haematoma and brain herniation; as it expands, the uncus of the temporal lobe herniates around the tentorium cerebelli.
376
What visual changes occur in extradural haemtoma?
Fixed dilated pupil
377
What is the definitive imaging in an extradural haemorrhage?
CT head
378
What does a CT head reveal in an extradural haemorrhage?
Biconcave (lentiform) and hyperdense collection around the surface of the brain
379
What is the definitive treatment of an extradural haemorrhage?
Craniotomy and evacuation of the haematoma
380
What are the symptoms of a cerebellar stroke?
Dysdiadochokinesia (an inability to perform rapid alternating hand movements)
Ataxia (a broad-based, unsteady gait)
Nystagmus (involuntary eye movements)
Intention tremor (seen when the patient is asked to perform the 'finger-nose test')
Slurred speech
Hypotonia
381
What is Weber's syndrome?
A midbrain stroke characterised by a third cranial nerve palsy and contralateral motor weakness (hemiparesis)
382
Which cranial nerve is affected in Weber's syndrome?
Third cranial nerve
383
What is the main cause of basal ganglia haemorrhages?
Hypertension
384
What type of aneurysms are associated with a subarachnoid haemorrhage?
Charcot-Bouchard
| Berry aneurysm - Predominantly
385
Which class of drugs are associated with worsening Myasthenia Gravis?
beta-blockers
386
What is the first stage of thiamine deficiency in chronic alcoholism?
Wet/Dry beriberi
387
Which factor is associated as a worse prognosis for a patient with MS?
Male sex
388
Which anti-epileptic drug is administered in a tonic-clonic seizure?
Lamotrigine
389
When should a patient take Sumatriptan during a migraine?
Once the headache starts and not during the aura phase
390
What is the first-line prophylactic management of a migraine?
Propranolol or amitriptyline or topiramate (Tetatrogenic)
391
Which migraine prophylaxis is contraindicated in women of child bearing age?
Topiramate
392
A mid-shaft humeral fracture is associated with injury to which peripheral nerve?
Radial nerve (runs along the radial groove)- causes wrist drop
393
A radial nerve palsy causes what?
Wrist drop
394
Tension headaches are associated with what type of tenderness?
Scalp muscle
395
Which gaze is associated with a progressive supranuclear palsy?
Vertical gaze - inability to look in vertical direction
396
A lesion to which artery is associated with Locked-in syndrome?
Basilar artery
397
In malignancy-associated spinal cord compression what i the management?
Dexamethasone
398
Which antibody is most common in myasthenia gravis?
Nicotinic acetylcholine receptor antibodies
399
A ring-enhancing lesion on a CT with a history of immunosuppressants is associated with what?
brain abscess
400
Lip-smacking is associated with what type of focal seizure?
Temporal lobe
401
What is the management of a warfarin-induced intracranial bleed?
Vitamin K 5mg IV and prothrombin complex concentrate
402
Hemiballism is associated with a lesion to which basal ganglia structure?
Sub-thalamic nucleus
403
Which part of the brain is an acoustic neuroma best visualised?
Cerebellopontine angle
404
What is the classical presentation of an acoustic neuroma?
The classical history of vestibular schwannoma includes a combination of vertigo, hearing loss, tinnitus and an absent corneal reflex. Features can be predicted by the affected cranial nerves:
cranial nerve VIII: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
cranial nerve V: absent corneal reflex
cranial nerve VII: facial palsy
405
The absent corneal reflex associated with tinnitus and vertigo is associated with what diagnosis?
Acoustic neuroma
406
What radiological imaging should be conducted in an acoustic neuroma?
MRI of the cerebellopontine angle
407
Which part of the ear is more sensitive to air conduction?
The inner ear is more sensitive to sound via air conduction than bone conduction
408
What tuning fork is used for the Rhinnes and Weber test?
512Hz
409
If a patient has unilateral conductive hearing loss, Weber's test would lateralise to which ear?
The affected ear
410
If a patient has unilateral sensorineural hearing loss, Weber's test would lateralise to which ear?
The normal ear
411
What is Rinne's test normal?
Air louder than Bone
| Rinne’s Positive
412
What is Rinne's negative?
Bone louder than Air (Conductive hearing loss)
413
What are the common causes of conductive hearing loss?
cerumen impaction, otitis media, and otosclerosis.
414
What is normal Weber test?
Sound is heard in the midline
415
Why is the COCP contraindicated in migraines?
Significantly increased risk for developing a stroke
416
What categories are associated with a partial anterior circulation stroke?
Two of the following:
Contralateral motor deficit
Homonymous hemianopia
Higher cortical dysfunction
417
What categories are associated with a total anterior circulation stroke?
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia
418
A III cranial nerve palsy with an enlarged pupil is associated with what type of cause?
surgical third nerve palsy, most likely caused by external compression due to a tumour
419
What is the definition of multiple sclerosis?
A chronic inflammatory multifocal demyelinating disease of the central nervous system.
-Loss of myelin and oligodendroglian and aonal pathology
420
What is the most common type of multiple sclerosis?
Relapsing remitting
421
What are the signs of multiple sclerosis?
```
Optic neuritis
Sensory disturbance
Hemiparesis/hemisensory loss
Motor weakness
Fatigue
Lhermitte's sign
Hyperreflexia and spasticity
Urinary urgency and incontinence
Diplopia
Vertigo
Visual feed defect
Dysarthria
```
422
What CSF findings are associated with MS?
Oligoclonal bands
423
What scan is used for MS?
Gadolinium contrast scan
424
What autoantibodies are associated with myasthenia gravis?
Against AChR at NMJ
425
What is associated with myasthenia gravis (manifestation)?
Thmus association
Thymic hyperplasia
Thymoma
426
What is the presentation of MG?
```
Ptosis
Diplopia
Dysarthria
Dysphagia
SOB
Fatigable muscles
Normal reflexes
```
Muscle fatigue with use
427
What is elevated in MG BLOOD?
Anti ACHr And anti-Musk antibodies
428
What does an EMG reveal in MG?
Decline in amplitude with repetitive use of muscle
429
What antibodies are associated w Lambert Eaton Mysathetnic syndrome?
autoantibodies against presynaptic VGCC at NMJ
430
What is the presentation of LEMS?
Difficulty walking
Weakness in upper arms and shoulder
Dry mouth
Constipation
Incontinence
Muscle weakness improves with use
Hyporeflexia
Associated with small cell lung cancer
431
LEMs is associated with which type of lung cancer?
Small cell lung cancer
432
What are the symptoms of MND?
Progressive muscle weakness
Dysphagia
Shortness of breath
Sparing of oculomotor, sensory and autonomic function
-Wasting of thenar muscles and tongue base
433
Signs of uMn Lesion
Spasticity
Hyper-reflexia
Clonus
Positve Babinski's sign
434
Sign of LMN
Hyporeflexia
Hypotonia
Muscle atrophy
Fasciculations and fibrillations
435
What is Parkinson?
Loss of dopaminergic neurones in the substania nigra (Midbrain)
436
What is the triad of parkinsons
Bradykinesia
Resting tremor and
Rigidity
437
Which drugs can cause Parkinsonian features?
Anti-emetics
| Anti-pyschotics
438
What are the 6Ms of Parkinon's?
```
Monotonous hypotonic speech
Micrographia
March a petit pas
Misery (depression)
Memory loss (dementia)
HypoMesis
```
439
What gait is associated with Parkinson's?
Shuffling gait
440
What palsy is associated with progressive supranuclear palsy?
Vertical gaze
441
Where does Huntington;'s disease affect?
Straitum (caudate and putamen)
442
Inheritance pattern of Huntington’s Disease?
Autosomal dominant pattern
| CAG trinucleotide
443
Symptoms of Huntington’s Disease
Chorea
Athetosis - slow involuntary and writhing movements
Dysphagia
Ataxia
```
Cognitinve
-Depression
-Personality changes
Lack of concentration
Dementia
```
444
What genetic testing is done in Huntington’s Disease?
CAG repeat testing
445
Triad of Wernicke's
Ataxia
Eye signs - opthahlmoplegua, nystagmus, diplopia and ptoss
Confusion
446
Common cause of encephalitis (Virus)
Herpes simplex virus
447
Management of stroke within 4.5 hours?
Thrombolysis (IV atelplase) and thrombectomy
448
Management of stroke within 6 hours
Thrombectomy
449
Middle finger dermatome
C7
450
Management of Parkinson's if motor function is affecting QoL?
Levodopa
451
Cause of non-communicating hydrocephalus
Arnold-chiari malformation
452
Main features of Neuroleptic malignant syndrome
rigidity, hyperthermia, autonomic instability (hypotension, tachycardia) and altered mental status (confusion)
453
What are the causes of pre-chiasmal visual field defects (One eye is affected, ipsilatearl)
```
Optic neuritis
Amaurosis fugax
Optic atrophy
Retrobulbar optic neuropathy
Trauma
```
454
What are the main causes of bitemporal hemianopia?
Pituitary adenoma
| Suprasellar aneurysm
455
What are the causes of homonymous contralateral hemianopia?
Stroke
Tumour
Trauma
456
Which interocular muscles are innervated by the oculomotor nerve?
Superior rectus
Inferior rectus
Medial rectus
Inferior oblique
457
Which extra-ocular muscle is innervated by the trochlear nerve?
Superior oblique
458
Which extra-ocular muscle is innervated by the abducens nerve?
Lateral rectus
459
What is the presentation of an oculomotor palsy?
Ptosis
Mydriasis
Down and out
460
What is the presentation of a trochlear nerve palsy?
Prevents moving inwards and down
461
What is the presentation of an abducens nerve palsy?
Prevents movement outwards
462
Which virus is associated with Ramsay Hunt syndrome?
Reactivation of varicella zoster
463
What is the triad of Horner's syndrome?
Miosis
Partial ptosis
Anhidrosis
464
What tumour is associated with Horner syndrome?
Pancoast tumour
465
Which chromosome is associated with neurofibromatosis type 1?
Chromosome 17
| Mutation in neurofibromin
466
What skin manifestation is associated with NF?
Cafe au lait macules
467
What is the presentation of neurofibromatosis?
Signs of hydrocephalus, brain tumours
Cerebellor abmnormalities
Seizures
468
What is the investigation for neuroplastic spinal cord compression?
Urgent Spinal MRI
469
What is a significant complication of spinal mets?
Neuroplastic spinal cord compression
470
What is the treatment for neuroplastic spinal cord compression?
High-dose oral dexamethasone
