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Neurology Flashcards

1
Q

Examples of primary headaches ?

A

Migraine
Tension headache
Clusher headache

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2
Q

What are secondary headaches ?

A

Headaches caused by a medication or medical illness

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3
Q

What are red flag symptoms for secondary headaches ?

A

HIV or immunosuppressed patients
Fever
Thunderclap headache
Seizure with new headache
Suspected meningitis, encephalitis
Acute glaucoma
Papilloedema

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4
Q

What is the most common cause of headache?

A

Medication overuse

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5
Q

What is a tension headache?

A

Generalised facial pain involving frontal and occipital region described as a tight band across the head

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6
Q

How can tension headaches be classified?

A

Episodic; less than 15 days per month
Chronic; More than 15 days per months for 3 months

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7
Q

What is the epidemiology for tension headaches?

A

Most common primary headache
2:3 male to female ratio
Onset between 20 and 30 years

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8
Q

What is the pathophysiology of tension headache ?

A

Release of inflammatory agents leads to sensitisation of peripheral trigeminal afferents leading to central hypersensitivity
Noicicentor is pericranial musculture
Chronic headaches lead to generalised hyperalgesia

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9
Q

Risk factors for tension headaches ?

A

Stress
Mental tension
Hunger
Sleep deprivation
Fatigue
Bad posture
Eye strain
Anxiety
Depression
Missed meals
Noise

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10
Q

What is the clinical presentation of tension headache?

A

Bilateral, pressure-like, non-throbbing and constricting pain
Dull non-pulsatile symptoms of varying intensity
Worsen as day progresses
Symptoms not aggravated by physical activity
Pressure behind eyes

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11
Q

How long does a tension headache last?

A

30 minutes to 7 days

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12
Q

Differentials to consider in tension headache?

A

Chronic migraine
Medication overuse headache
Sphenoid sinusitis
Giant cell arteritis
Temporomandibular joint disorders
Pituitary/brain tumour
Chronic subdural haematoma

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13
Q

Investigations for tension headaches?

A

Clinical diagnosis based on history and examination findings, headache diary

Investigations to rule out other causes

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14
Q

What investigations can be done to rule out differentials of tension headaches?

A

CT sinus; exclude spheroid simisitis
MRI brain; exclude brain tumour
Lumbar puncture; infection, sinus venous thrombosis

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15
Q

What is the management for episodic tension headache?

A

Over the counter simple analgesia ( Paracetamol, aspirin, NSAID)
Assess and manage triggers

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16
Q

What is the management of chronic tension headache?

A

6-10 sessions of acupuncture
Physiotherapy and regular exercise
CBT and relaxation techniques
10mg Amitriptyline prophylaxis

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17
Q

Which medication should not be used in treatment of tension headache?

A

Opioids

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18
Q

Complications of tension headache?

A

Impact on quality of life
Depression and low mood
Medication overuse causing more headache

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19
Q

What is a migraine?

A

Recurrent, throbbing headache preceded by aura and associated with nausea, vomiting and visual changes

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20
Q

What is the epidemiology of migraines ?

A

More common in females
90% of cases have onset before 40
Severity decreases with increasing age
Affects 1 in 6 patients
Most common cause of episodic headache

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21
Q

What is the most common cause of episodic headache?

A

Migraine

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22
Q

What are the trigger for migraine?

A

Chocolate
Hangover
Orgasm
Cheese
Oral contraceptives
Lie -ins
Alcohol
Tumult
Exercise

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23
Q

What is the aetiology of migraines ?

A

Any of the triggers
Brain chemical imbalance
Changes in brainstem and interactions with trigeminal nerve

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24
Q

What is the pathophysiology of migraines?

A

Neuronal and glial depolarisation spreads across cerebral cortex causing migraine aura and release of inflammatory mediators
Neurogenic inflammation of first division of trigeminal sensory neurones which innervate large vessels and meninges . releases substances causing dilation of blood vessels, leakage of plasma proteins into surround tissue and pain
These changes lead to unstable trigeminal nerve nucleus

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25
What is the clinical presentation of migraine?
Headache lasting 4-72 hours Unilateral throbbing pain Nausea and vomiting Decreased ability to function Headache worsens with activity Photophobia, phonophobia
26
What are the components of aura?
Positive phenomena; Visual sparkles, flashing lights Negative cnomena; Visual loss, scotoma Sensory aura; Numbness and tingling
27
What investigations can be used to diagnose migraines?
Clinical diagnosis; headache diary can be helpful to identify pattern ESR; rule out temporal arteritis Lumbar puncture; infection MRI brain; space occupying/ischaemic lesion CT head; intracranial haemorrhage Fundoscopy; papilloedema
28
What are the differentials for migraines?
Other primary headache Subarachnoid haemorrhage Cerebral neoplasm Temporal arteritis Arterial dissection Ischaemic stroke
29
What is the acute management for migraine?
Simple analgesia; Ibuprofen, Aspirin, Paracetamol Triptan medication; Sumatriptan Antiemetic; Prochlorperazine, Metoclopramide
30
What is prophylactic therapy for migraine?
Propanolol Topiramate Amitriptyline Acupuncture and behavioural intervention
31
Which medication should not ble ased in migraines?
Opioids
32
What monitoring is required for migraine?
2-8 weeks from starting treatment
33
What are the complications of migraine?
Migrainous infarction Depression Cardiovascular disease Chronic migraine Complications of pregnancy
34
What is the prognosis of migraines?
Patients cope well with diagnosis Impact on quality of life and ADL
35
What is a cluster headache?
Rare and severe headache associated with unilateral excruciating pain
36
What is the most disabling primary headache?
Cluster headache
37
What is the epidemiology of cluster headache ?
More common in males Age of onset between 20 and 40 years 90% episodic and 10% chronic
38
What is the aetiology of cluster headaches?
Autosomal dominant gene association Environmental influence
39
What are the risk factors for cluster headaches?
Head trauma Heavy alcohol intake and smoking Family history Male sex Sleep apnoea
40
What is the pathophysiology of cluster headache?
Trigeminal autonomic reflex causes pain and autonomic features of attack
41
What are the cardinal features of cluster headache?
Trigeminal distribution of pain Ipsilateral cranial autonomic symptoms Circadian pattern of attack
42
Clinical presentation of cluster headaches?
Repeated attack of unilateral, periorbital excruciating pain Lacrimation, conjunctival injection Rhinorrhoea Agitation and restlessness Partial horner's syndrome Nausea, vomiting Photophobia, phonophobia, Migrainous aura
43
Investigations used to diagnose cluster headaches?
Clinical diagnosis based on history Brain MRS; rule out tumour, cavernous sinus pathology ESR; Giant call arteritis Pituitary function test; pituitary adenoma
44
What are differential diagnosis for cluster headache?
Migraine Paroxysmal berniciavia Trigeminal neuralgia Cluster-tic syndrome Subarachnoid haemorrhage
45
What is the acute management for cluster headache?
Sumatriptan - SC/nasal High flow 100% oxygen at flow rate of 12-15 L/ min via non rebreathable Mask for 15-20 minutes
46
What is the prophylactic therapy for cluster headache?
Verapamil Corticosteroid Avoid smoking /drinking
47
What is the monitoring requirement for cluster headache?
See neurologist ECG, TFT, U+E for those on lithium
48
What are the complications of cluster headaches?
Depression Poor quality of life
49
What is trigeminal neuralgia?
Facial pain syndrome in distribution of one or more divisions of the trigeminal nerve with no neurological deficit
50
What is the epidemiology of trigeminal neuralgia?
More common in females Peak age between 50 and 60 years Prevalence increases with age 20 times more prevalent in patients with MS
51
What medical condition is associated with trigeminal neuralgia?
Multiple sclerosis
52
What is the primary cause of trigeminal neuralgia?
Intracranial vascular compression
53
What are secondary causes for trigeminal neuralgia?
Pathology in brainstem; tumour MS, infarction Pathology at cerebellopontine angle; acoustic neuroma, tumour Pathology within petrous bone; middle ear infection Pathology within cavernous sinus; Aneurysm of internal caratic, tumour, thrombosis of cavernous sinus
54
What is the pathophysiology of trigeminal neuralgia?
Compression of trigeminal nerve root at the root entry zone by aberrant vascular loop Typically superior cerebellar artery Results in focal demyelination and resultant conduction aberrations result in neuropathic pain
55
Risk factors you trigeminal neuralgia?
Hypertension Multiple sclerosis Increasing age Female
56
What is the clinical presentation of trigeminal neuralgia?
Pain in trigeminal distribution, recurring and paroxysmal pair, intense, sheurp, superficial stabbing unilateral pain Pain lasts seconds the minutes
57
What is needed for a diagnosis of trigeminal neuralgia?
Atleast 3 attacks of unilateral facial pain
58
What are triggers for trigeminal neuralgia?
Facial /oral mechanical stimulation e.g tooth brushing, eating, cold, washing area, eating, talking, shaving, dental prostheses
59
Investigations for trigeminal neuralgia?
Clinical diagnosis based on history Trigeminal reflex test ; Early blink reflex or early masseter reflex Intra-oral reflex the rule out dental cause MRI scan
60
Differential diagnosis in trigeminal neuralgia?
Dental caries Dental fractures Mandibular osteomyelitis TMJ syndrome Migraine Temporal arteritis Glossopharyngeal neuralgia
61
What medications are used in trigeminal neuralgia?
Carbamazepine Phenytoin, gabapenting lamotrigine; less effective and should be started by specialist
62
Which mediations are not effective in trigeminal neuralgia?
Typical analgesic, opioids
63
What is the management if medications fail in trigeminal neuralgia?
Microvascular decompression; anomalous vessel separated from trigeminal nerve root Gamma knife surgery Stereotactic radiosurgery
64
What is giant cell arteritis?
Immune mediated granulomatous vasculitis of large/ medium sized arteries
65
What is the epidemiology of giant cell arteritis ?
Most common form of systemic vasculitis More common in females over age of 50 years More common in white, North European ancestry
66
What is the aetiology of giant cell arteritis?
Genetics; Polymorphism of HLA class II region Infection; Mycoplasma Pneumoniae, parovirus B 19, parainfluenza virus, chlamydia pneumonia, varicella zoster
67
What is the pathophysiology of giant cell arteritis?
Immune insult to adventitia of arterial wall results in inflammation of artery Fragmentation of internal elastic lamina Inflammatory changes lead to vessel narrowing and occlusion which leads to ischaemia
68
Risk factors for giant cell arteritis?
Age over 50 years Increasing age Female sex Genetics Smoking Atherosclerosis Environmental factors
69
Clinical presentation of giant cell arteritis?
Severe pulsating temporal headache Scalp pain or tenderness Aching and stiffness Loss of vision/ abnormal fundoscopy Jaw pain and tongue claudication
70
Investigations for giant cell arteritis?
Elevated CRP and ESR Normocytic, normochromic anaemia Vascular ultrasound Temporal artery biopsy
71
What is seen on vascular ultrasound in giant cell arteritis?
Wall thickening Stenosis/ occlusion
72
What is seen on temporal artery biopsy in giant cell arteritis?
Granulomatous inflammation Multinucleated giant cells
73
Differentials for giant cell arteritis?
Polymyalgia rheumatica Solid organ cancer Haematological malignancy Takayasu’s arteritis Amyloidosis SLE Connective tissue disease
74
What is the treatment for giant cell arteritis?
High dose corticosteroids which are weaned over 12-24 months If visual symptoms persist give IV methylprednisolone for 3 days Long term bone and GI protection
75
What are the monitoring requirements for giant cell arteritis?
Every 2-8 weeks for first 6 months Every 12 weeks during second 6 months Every 12-24 weeks during second year Any point during relapse When glucocorticoid therapy is modified
76
What are the complications of giant cell arteritis?
Large vessel stenosis Aortic aneurysm Glucocorticoid related adverse effects Vision loss
77
What is the prognosis of giant cell arteritis?
Increased risk of aortic aneurysm and cardiovascular disease
78
What is a transient ischaemic attack?
Brief episode of neurological dysfunction caused by focal brain, spinal or retinal ischaemia without infarction with symptom lasting less than 24 hours
79
What is the epidemiology of TIA?
15% of first strokes are preceded by TIA More common in males Black ethnicity has a higher risk
80
Pathophysiology of TIA?
Cerebral ischaemia results in lack of oxygen and nutrients resulting in cerebral dysfunction with infarction of cerebral tissue
81
Aetiology of TIA?
In- situ thrombosis of intracranial artery Cardioembolic events; AF, impaired ejection fraction Small vessel occlusion; Microatheroma, hypercoaguability, dissection, vasculitis, vasospasm, sickle cell anaemia Hypoperfusion; cardiac arrhythmia, postural hypotension, decreased flow through narrowed artery
82
Risk factors for TIA/ stroke?
Male Family history Increasing age Atrial fibrillation Valvular disease Carotid stenosis Congestive heart failure Hypertension Diabetes mellitus Cigarette smoking Alcohol Hyperlipidaemia Patent foramen ovale Obesity Hypercoaguability Lack of exercise
83
What systems are used to classify TIA?
Bamford classification; Based on presenting symptoms and clinical signs TOAST criteria; Based on aetiology
84
What is the Bamford classification?
TIA classification based on presenting symptoms Total anterior circulation Partial anterior circulation Posterior circulation ( vertebrobasilar territory ) Lacunar
85
What is the TOAST criteria?
Classification system used for TIA based on aetiology Large artery atherosclerosis Cardio-embolism Small vessel occlusion Other determined aetiology ( Non atherosclerotic vasculopathy, haematological disorder ) Undetermined aetiology
86
What are the features of anterior circulation TIA?
Affects frontal and medial parts of cerebrum Weakness, paraesthesia in contralateral limb Hemiparesis Hemi sensory disturbance Dysphagia Amaurosis fugax
87
What percentage of TIA affect anterior and posterior circulation?
Anterior; 90% Posterior; 10%
88
What is the presentation of a posterior circulation TIA?
Diplopia Vertigo Vomiting Choking and dysarthria Ataxia Hemisensory loss Loss of consciousness Hemianopia vision loss Transient global amnesia Tetraparesis
89
What is the classical features of TIA?
Transient sudden sensory/ motor dysfunction No evidence of infarction on imaging
90
Investigations performed in TIA?
Blood glucose Bloods; FBC, coagulation screen ECG CT scan; look for evidence of infarction
91
Differentials for TIA?
Stroke Hypoglycaemia Todd’s paralysis Complex migraine Space occupying lesion Multiple sclerosis Peripheral neuropathy
92
Management for TIA?
Calculate ABCD2 score Loading dose aspirin Seen by specialist within 7 days Secondary prevention of stroke
93
What is secondary prevention of stroke following TIA?
Lifestyle counselling and risk factor optimisation Antiplatelet therapy; 75 mg clopidogrel Atorvastatin 20-80mg daily Anti hypertensives
94
What is ABCD2 score?
Age; over 60 years Blood pressure; > 140/90 Clinical presentation; Speech impairment (2 points), Unilateral weakness (1 point) Diabetes mellitus Duration; 10-59 minutes (1 point), >60 minutes (2 points)
95
Complications of TIA?
Stroke Myocardial infarction
96
Prognosis of TIA?
8% of patients will have a stroke following TIA hospitalisation Over 10% will have stroke within 3 months of TIA
97
What is a Stroke?
Rapid onset syndrome of neurological deficit caused by focal cerebral, spinal or retinal infarction Symptoms last over 24 hours
98
Epidemiology of stroke?
Incidence increases with age Higher in asian ethnicity Incidence is falling due to rigorous management of risk factors Trauma included stroke is common in younger patients
99
Aetiology of stroke?
Ischaemic stroke (80%) Haemorrhagic stroke (15%) Trauma Vasculitis
100
What is the pathophysiology of ischaemic stroke?
Blood supply in cerebral vascular territory is reduced, leading to irreversible cell death and infarction of cerebral tissue
101
What is the pathophysiology of haemorrhagic stroke?
Rupture of intracerebral vessel causes bleeding into brain parenchyma Expanding haematoma can sheer or occlude neighbouring arteries Results in raised ICP, cerebral hypoperfusion, and ischaemic injury
102
What is a Charcot-Bouchard aneurysm?
Microaneurysm caused by hypertension
103
Primary causes of intracerebral haemorrhage?
Idiopathic Anticoagulation
104
What are secondary causes of intracerebral haemorrhage?
Vasculitis Connective tissue disease Amyloid angiopathy Aneurysm
105
What is the presentation of an anterior cerebral artery stroke?
Leg weakness Sensory disturbance in leg Gait apraxia Truncal ataxia Incontinence Drowsiness Akinetic mutism
106
What is the presentation of a middle cerebral artery stroke?
Contralateral arm and leg weakness Contralateral sensory loss Hemianopia Aphasia Dysphagia Facial drop
107
What is the presentation of posterior cerebral artery stroke?
Contralateral homonymous hemianopia Cortical blindness Visual agnosia Prosopagnosia Unilateral headache
108
What is the presentation of a posterior circulation stroke?
Motor deficit; hemiparesis, tetraparesis, facial paralysis Dysarthria Vertigo, nausea, vomiting Visual.disturbance Altered conciousness
109
What is the presentation of a lacunar stroke?
Unilateral weakness Sensory deficit of face, arm, leg or all three Pure sensory loss Ataxic hemiparesis
110
In which stroke is patient more likely to get locked in?
Posterior circulation (Vertebrabasilar artery)
111
Investigations performed in stroke?
Bloods; FBC, U+E, glucose, LFT, clotting screen Non contrast CT head
112
What is seen on a non contrast head CT in ischaemic stroke?
Hypoattenuation of brain parenchyma Loss of grey matter
113
What is seen on a non contrast CT in a haemorrhagic stroke?
Hyperattenuation suggesting acute blood Surrounding hypoattenuation due to oedema
114
Differentials for stroke?
Transient ischaemic attack Hypertensive encephalopathy Hypoglycaemia Complicated migraine Subdural haematoma Wernicke encephalopathy Brain tumour Sepsis
115
What is the treatment of ischaemic stroke?
Maximise ischaemic tissue; fluids and maintain sats over 95% tPA thrombolysis within 4.5 hours of symptom presenting, followed by aspirin and clopidogrel for 2 weeks, then clopidogrel lifelong Mechanical thrombectomy
116
What is the management of haemorrhagic stroke?
Frequently monitor GCS Reverse pre- existing anticoagulation (vitamin K, beriplex) Control hypertension Manual decompression (mannitol) Decompressive surgery
117
What prophylactic measures are taken to prevent stroke?
Antiplatelet therapy ( aspirin + clopidogrel ) Cholestrol management Atrial fibrillation treatment and anticoagulation Blood pressure management
118
Contraindications for thrombolysis?
Recent surgery in last 3 months Recent arterial puncture History of active malignancy Evidence of aneurysm in brain Patient is on anticoagulation Severe liver disease Acute pancreatitis Clotting disorder Above 80 years
119
What is the alternative if clopidogrel is not tolerated?
dipyramidole
120
What parameters are monitored in stroke patients in hospital?
GCS Blood pressure Blood glucose Oxygen saturations Hydration Temperature Cardiac rhythm, rate Development of seizures
121
Complications of stroke?
Infection Seizures Deep vein thrombosis Delerium Aspiration pneumonia Alteplase related orolingual oedema Haemorrhagic transformation of ischaemic stroke
122
Prognosis of stroke?
Leading cause of serious long term disability Patients treated with alteplase have better functional outcome
123
What is a subarachnoid haemorrhage?
Spontaneous bleeding into subarachnoid space
124
Epidemiology of subarachnoid haemorrhage?
Accounts for 5% of strokes Decreasing incidence due to better management of risk factors Incidence increases with age
125
Aetiology of subarachnoid haemorrhage?
Spontaneous rupture of intra-cranial saccular berry aneurysm Arteriovenous malformations Bleeding disorders Anticoagulation use Acute bacterial meningitis Tumours
126
What is the pathophysiology of subarachnoid haemorrhage?
Cerebral aneurysm arises at the bifurcation of arteries in the circle of willis Weaking in the arterial walls increases risk of rupture Rupture leads to bleeding into subarachnoid space
127
Risk factors for subarachnoid haemorrhage?
Hypertension Smoking Family history ADPKD Alcohol/ Cocaine use Marfans/ Ehlers-Danlos syndrome Neurofibromatosis type I
128
Clinical presentation of subarachnoid haemorrhage?
Sudden onset headache (thunderclap) Reduced/ loss of consciousness Neck stiffness Eyelid drooping, diplopia, mydriasis, orbital pain Papilloedema Kernig sign Brudzinski sign
129
What is Kernig sign?
Unable to extend leg at knee when thigh is flexed
130
What is Bridzinski sign?
When neck is flexed by doctor, patient will flex knees and thighs
131
Investigations performed in subarachnoid haemorrhage?
Urgent non contrast CT of head Lumbar puncture CT cerebral angiogram Bloods, ECG
132
What is seen on non contrast CT in subarachnoid haemorrhage?
Hyperdense star shaped lesion in subarachnoid space
133
What is seen on lumbar puncture in subarachnoid haemorrhage?
Xanthochromia, 12 hours after symptom onset
134
What are the differentials for subarachnoid haemorrhage?
Non-aneurysmal perimesencephalic SAH Arterial dissection AV malformation Vasculitis Anticoagulation use Migraine Cortical vein thrombosis
135
What is the management for subarachnoid haemorrhage?
Maintain cerebral perfusion; IV fluids and keep blood pressure below 160mmHg Nimodipine to reduce vasospasm Mannitol to prevent raised ICP Endovascular coiling/ clipping Surgery
136
What are the monitoring requirements for subarachnoid haemorrhage?
If aneurysmal disease then frequency and imaging modality is determined on a case basis
137
Complications of subarachnoid haemorrhage?
Neuropsychiatric problems Chronic hydrocephalus
138
Prognosis of subarachnoid haemorrhage?
Responsible for 1/3 of premature deaths Highest mortality in black and female patients Poor quality of life and reduced functional capabilities
139
What is a subdural haemorrhage?
Bleeding between dura mater and arachnoid mater of the meninges following rupture of bridging veins between cortex and venous sinus
140
Epidemiology of subdural haemorrhae?
More common in people with small brains (elderly, alcoholics and babies) Incidence increases with age
141
What is the aetiology of subdural haemorrhage?
Trauma, usually deceleration injury Dural metastasis Venous malformation
142
What is the pathophysiology of a subdural haemorrhage?
Torsion, sheering forces causes causes disruption of bridging cortical veins that empty into dural venous sinus and formation of haematoma . As haematoma gorwns the rise in pressure is able to stop bleeding. After a few days haematoma starts to autolyse and an increase in oncotic pressure raises ICP over couple of weeks
143
What is the consequence of raised ICP?
Leads to midline shift of structures Tectorial herniation and coning
144
Risk factors for subdural haemorrhage?
Traumatic head injury Cerebral atrophy Increasing age Alcoholism Male Physical abuse, shaken baby syndrome
145
What is the classification of subdural haematoma?
Acute subdural haematoma; less than 3 days old, diffusely hyperdense Subacute subdural haematoma; 3-21 days old, heterogeneously hyperdense/ isodense Chronic subdural haematoma; more than 21 days, diffusely hypodense Acute on chronic subdural haematoma; areas of hyperdensity with hypodense haematoma
146
What is the clinical presentation of subdural haematoma?
Recent trauma Headache Nausea/ vomiting Diminished eye/ motor response Confusion Focal neurology Stupor/ coma
147
Investigations in subdural haemorrhage?
Non contrast CT MRI
148
What is seen on non contrast CT in subdural haemorrhage?
Crescent shaped collection Hyperdense -> isodense -> hypodense May be a midline shift if raised ICP
149
What is the treatment for subdural haemorrhage?
Assess ABCDE and monitor GCS Mannitol to reduce ICP Neurosurgical management irrigation/ evacuation via burr hole craniotomy
150
Monitoring requirement for subdural haemorrhage?
Follow up CT 1-2 months post discharge Consult cardiology for when to restart anticoagulation
151
Complications of subdural haemorrhage?
Neurological deficit Coma Stroke Surgical site infection Epilepsy Recurrence of subdural haematoma
152
What factors are associated with a poorer prognosis in subdural haemorrhage?
Older age Greater severity of injury Low GCS Midline shift on imaging Early need for surgery Raised ICP
153
What is an extradural haemorrhage?
Acute haemorrhage between dura mater and the bone usually caused by head injury
154
What is the epidemiology of extradural haemorrhage?
Usually occurs in young adults, common in males aged 20-30 years 75% of cases are a result of skull fractures
155
What is the aetiology of extradural haemorrhage?
Skull trauma in temporoparietal region Ruptured middle meningeal artery, vein AV malformations Bleeding disorder
156
Pathophysiology of extradural haemorrhage?
Vessel damage leads to bleeding between dura mater and cranium As volume of blood in extradural space increases it begins to pull dura away from skull Can lead to raised ICP
157
Risk factors of extradural haemorrhage?
Trauma Male Young age
158
Clinical presentation of extradural haemorrhage?
Headache Nausea and vomiting Confusion Loss of consciousness Lucid interval Confusion, reduced GCS Neurological, sensory and motor deficits Cushing's triad Babinski sign
159
Investigations to diagnose extradural haemorrhage?
Bedside glucose and ECG Blood work; FBC, U+E, CRP, Coagulation, Group and save Imaging; CT, MRI, cerebral angiography
160
What is seen on CT in extradural haemorrhage?
Bi-convex lemon shaped mass Secondary features; midline shift, brainstem herniation
161
Differentials for extradural haemorrhage?
Epilepsy Carotid dissection CO poisoning Subdural haematoma Subarachnoid haemorrhage Meningitis
162
Management in extradural haemorrhage?
ABCDE, correction of anticoagulation, mannitol Surgical management
163
Monitoring requirement in extradural haemorrhage?
Serial scans to monitor ICP Close observation post operatively
164
Complications of extradural haemorrhage?
Infection Cerebral ischaemia Seizures Cognitive impairment Hemiparesis Hydrocephalus due to ventricular obstruction Brainstem injury
165
Factors that worsen prognosis following extradural haemorrhage?
Low GCS at presentation No history of lucid interval Pupil abnormalities Pre-existing brain injury
166
What is multiple sclerosis?
Chronic auto-immune T-cell mediated inflammatory demyelinating disease resulting in episodic neurological dysfunction in at least 2 areas of the CNS separated in time and space
167
What cells are attacked in MS?
Oligodendrocytes
168
What is the epidemiology of MS?
More common in females Most common age at diagnosis is 20-40 years More prevalent in European countries
169
Aetiology of MS?
EBV exposure Low sunlight exposure and Vit D deficiency
170
Pathophysiology of MS?
Infection/ metabolic stress triggers inflammatory response Activated T-cells seek entry into CNS via attachment to receptor on endothelial cells and td enter trough BBB Once in BBB inflammatory cascade causes destruction of oligodendrocytes
171
Where are demyelinating placques in MS likely to be found?
Optic nerve Ventricles of the brain Corpus callosum Brainstem and cerebellar connections Cervical cord
172
What are the types of MS phenotypes?
Relapsing Relapsing remitting Primary progressive Secondary progressive
173
What s the most common MS phenotype?
Relapsing remitting
174
Risk factors for MS?
Female Lack of sunlight/ vitamin D Exposure to EBV Northern latitude Smoking Personal/ family history of auto-immune disease Obesity
175
Clinical presentation of MS?
Unilateral optic neuritis Numbness or tingling of limbs Leg weakness Brainstem demyelination Cerebellar symptoms Trigeminal neuralgia Constipation Spasticity and weakness Bladder and sexual dysfunction Lhermitte's sign Cognitive decline
176
What is the presentation of optic neuritis?
Pain in one eye on movement Greying/ blurring of vision Reduced central vision
177
What are symptoms of brainstem demyelination?
Diplopia, vertigo, facial weakness, dysarthria, dysphagia Clumsy Loss of proprioception
178
What is Lhermitte's sign?
Electric shock like sensation extending down
179
What evidence is needed in history to diagnose MS?
Two or more attacks Affecting different parts of the CNS disseminated in time and space
180
Investogations performed in MS?
Bloods to rule out differentials; FBC, CRP, U+E, glucose, HIV serology, auto-antibodies, Ca2+, B12 MRI Lumbar puncture Electrophysiology
181
What is seen on MRI in MS?
Demyelinating lesions in spinal cord Hyperintensities in periventricular white matter in brain
182
What is seen in lumbar puncture in MS?
Oligoclonal IgG bands in 90% of cases CSF cell count
183
Differentials for MS?
Myelopathy Fibromyalgia Sleep disorder Sjorgens syndrome B12 deficiency Ischaemic stroke Lymphoma GBS ALS SLE
184
What is the management for MS?
Lifestyle management Regular exercise Smoking cessation Optimise co-morbidities Yearly flu vaccine Fertility and pregnancy counselling Managing relapse Methylprednisolone for 5 days SC interferon 1B or 1A Disease modifying agents; alemtuzumab, natalizumab, dimethyl fumarate Symptom management; physiotherapy, baclofen, tizanidine, botox Stem cell therpay can be considered
185
Monitoring requirements for MS?
Frequency of monitoring depends on patient situation, commonly every 6-12 months
186
Complications of MS?
UTI Osteopenia, osteoporosis Depression Visual impairment Cognitive impairment Impaired mobility
187
What is the prognosis of MS?
Life expectancy is reduced by 5-10 years Often die from aspiration pneumonia
188
What is myasthenia gravis?
Chronic autoimmune disorder against nicotinic acetylcholine receptors in the postsynaptic membrane of neuromuscular junction
189
Epidemiology of Myasthenia gravis?
More common in females Women present under 40 years and men over 60 years Increasing prevalence, especially in developed countires
190
Aetiology of Myasthenia gravis?
Antibody mediated autoimmune destruction Transient symptoms can be caused by D-penicillamine treatment for Wilsons disease
191
Risk factors for Myasthenia gravis?
Autoimmune conditions; Pernicious anaemia, SLE, rheumatoid arthritis Thymic hyperplasia Family history of Myasthenia gravis/ autoimmune conditions Cancer therapy
192
Pathophysiology of Myasthenia gravis?
Anti-AChR autoantibodies result in complement mediated destruction of postsynaptic membrane of neuromuscular junction Reduced number of binding sites available for ACh resulting in inconsistent generation of muscle fibre action potentials and manifesting as skeletal muscle weakness
193
What is the classification of Myasthenia gravis?
Class I; eye muscle weakness, ptosis, all other muscle strength is normal Class II; mild weakness of other muscles and eye muscle weakness of any severity Class III; moderate weakness of other muscles and eye muscle weakness of any severity Class IV; severe weakness of other muscles and eye muscle weakness of any severity Class V; need intubation to maintain airway
194
Clinical presentation of Myasthenia gravis?
Increasing muscle fatigue Ptosis, diplopia Myasthenic snarl on smiling Respiratory difficulties in generalised myasthenia gravis Fatigable tendon reflexes Proximal limb weakness
195
Weakness is myasthenia gravis worsens in which situations?
Pregnancy Hypokalaemia Infection Exercise Drugs; opiates, beta-blockers, gentamycin, tetracycline
196
What is seen on examination in myasthenia gravis?
When asked to count to 50, voice will become less audible When asked to focus on finger after a while patient will be unable to hold their vision
197
Investigations performed in Myasthenia gravis?
Serum anti-AChR (if negative look for anti-MuSK) EMG and nerve conduction studies CT scan of thymus to look for hyperplasia
198
Differentials for Myasthenia gravis?
Lambert-Eaton myasthenic syndrome Botulism Penicillamine induced myasthenia gravis Primary myopathies
199
Management in Myasthenia gravis?
Thymectomy if onset is over 50 years and poorly controlled symptoms Pyridostigmine for symptoms control Immunosuppression with steroids and azathioprine/ methotrexate
200
What is the management in myasthenic crisis?
Intubation Plasmapheresis and IVIG Steroids
201
Monitoring requirements for Myasthenia gravis?
Every 3-12 months depending on situation Blood work if immunosuppressed Lung function tests Assess for symptoms affecting ADL, difficulties with swallowing/ breathing, and effect of medications
202
Complications of Myasthenia gravis?
Pyridostigmine induced reactions Respiratory failure Impaired swallowing Acute aspiration Secondary pneumonia Cardiac complications Pregnancy complications
203
Prognosis of Myasthenia gravis?
Older patients, with poorer response to therapy and multiple co-morbidities have poorer prognosis
204
What is meningitis?
Inflammation of the meninges caused by bacterial, viral or fungal infection
205
What is the epidemiology of meningitis?
Occurs in all age groups More common in infants, young children and elderly Immunisation routine has changed epidemiology and incidence rates Viral meningitis is more common in men
206
Aetiology of meningitis?
Bacterial; Streptococcus pneumoniae is most common cause worldwide, Neisseria meningitidis is predominant in Europe Viral; Human enterovirus is most common cuase, HSV-2, varicella zoster Fungal
207
What is a common causative agent for meningitis in pregnant women?
Listeria monocytogenes
208
What is a common causative agent for meningitis in neonates?
Group B haemolytic streptococcus
209
Pathophysiology of bacterial meningitis?
Bacteria reach CNS and multiply in subarachnoid space Bacterial components in CSF induce an inflammatory response This leads to cerebral oedema, raised ICP contributing to neurological damage
210
What is the pathophysiology of viral meningitis?
Virus enters through faeco-oral route and virus replicates in non CNS tissue The virus is carried to CNS by haematological spread and enters subarachnoid space leading to inflammatory response and meningitis
211
Risk factors for meningitis?
Genetic predisposition Advancing age Crowding; military base, university students Intrathecal access Immunocompromised patients; HIV, malignancy, asplenia, congenital Exposure to pathogens Bacterial endocarditis IVDU Sickle cell disease Diabetes
212
Clinical presentation of meningitis?
Headache Neck stiffness Fever Altered mental status Nausea, vomiting Photophobia Seizures Petechial non blanching rash Papilloedema Kernig's sign Brudzinski's sign
213
Investigations in meningitis?
Blood culture Serum PCR Bloods; FBC, U+E, CRP, VBG, LFT, coagulation screen Lumbar puncture; CSF protein/ cells/ glucose, microscopy and gram staining, lactate, viral serology
214
What is the CSF findings in bacterial meningitis?
Polymorph neutrophils Raised protein Low glucose
215
What is the appearance of CSF in bacterial infection?
Turbid
216
What are the CSF findings in viral meningitis?
Lymphocytes Normal protein count Normal glucose
217
What are the indications for LP?
Age over 60 Immunocompromised History of CNS disease New onset seizures Decreasing GCS Focal neurological signs Papilloedema
218
Differentials for meningitis?
Encephalitis Toxic/ metabolic encephalitis Drug induced meningitis Tuberculous meningitis Intracranial haemorrhage
219
Management of bacterial meningitis?
Transfer patient to hospital Administer stat dose of IM benzylpenicillin Once causative agent has been identified give appropriate antibiotic course Consider steroids to reduce cerebral oedema Give Ciprofloxacin to close contacts
220
What is the antibiotic course for Strep.pneumoniae, Haemophilus influenzae meningitis?
Ceftriaxone/ cefotaxime for 10 days
221
What is the antibiotic course for listeria monocytogenes?
Amoxicillin for 21 days
222
What is the antibiotic course for staphylococcus aureus meningitis?
Flucloxacillin for 14 days
223
What is the management for viral meningitis?
Supportive management Consider acyclovir
224
Complications of bacterial meningitis?
Shock Raised ICP Hydrocephalus Cognitive, behavioral and academic problems Seizures Subdural effusion Hearing loss
225
Complications of viral meningitis?
Persistent headache and malaise Neurodevelopmental deficits in infants
226
Prognosis in meningitis?
Excellent with therapy Poorer prognosis is associated with increasing age, co-morbidities, causative pathogen, severity of presentation, low GCS
227
What is encephalitis?
Infection and inflammation of the brain parenchyma
228
Epidemiology of encephalitis?
Bimodal age distribution (below 1 year and over 65 years) More common in immunocompromised
229
Aetiology of encephalitis?
Viral is most common Bacterial Fungal Auto-immune
230
Pathophysiology of encephalitis?
Causative agents induces inflammation in brain tissue resulting in neurological dysfunction
231
Risk factors for encephalitis?
Young and elderly Immunocompromised Geographic location Smoking Autoimmune disease Seasonal changes
232
Clinical presentation of encephalitis?
Features of viral illness; Fever, myalgia, headache, nausea Progresses to; Personality and behavioral change Decreased consciousness Focal neurological deficit Seizures Raised ICP
233
Investigations for encephalitis?
Blood tests; FBC, U+E, LFT Blood film to detect malaria Throat swab and sputum culture MRI Lumbar punture
234
What is seen on MRI in encephalitis?
Inflammation and swelling of brain parenchyma Midline shift in context of raised ICP
235
Differentials for encephalitis?
Meningitis Stroke Brain tumour Toxic/ metabolic encephalopathy Intracranial bleed
236
Management of encephalitis?
Supportive care and monitor vitals IV acyclovir for viral aetiology
237
Monitoring requirements in encephalitis?
Neuropsychological testing in childhood survivors due to increased risk of ADHD and cognitive problems
238
Complications of encephalitis?
Death Hypothalamic and autonomic dysfunction Ischaemic stroke Seizures Cerebral haemorrhage Cerebral vasculitis Neurodevelopmental problems
239
Prognosis of encephalitis?
Based on aetiology Older age, decreased consciousness, delayed treatment associated with poorer prognosis
240
What is a brain abscess?
Suppurative collection of microbes within gliotic capsule occurring within brain parenchyma
241
What is the epidemiology of brain abscess?
Highest prevalence in adult men under 30 years In children common between 4-7 years More common in men Most common cause of space occupying lesion worldwide
242
What is the aetiology of brain abscess?
Infection with bacterial, fungal, parasitic organisms
243
Pathophysiology of brain abscess?
Originate in ischaemic white matter adjacent to cortex Entry of infective organism through haematogenous spread Early cerebritis (3 days); local inflammation, tissue necrosis, neutrophilic infiltration, activation of microglia and astrocytes Late cerebritis (day 4-9); increased organisation where lymphocytic and microglial infiltration Frank abscess; encapsulation, suppurative collection
244
Risk factors for brain abscess?
Immunocompromised Cancer/ chronic illness Congenital heart disease Major head trauma, surgery or injury Meningitis Chronic sinus or middle ear infection IVDU Diabetes mellitus Infective endocarditis
245
Clinical presentation of brain abscess?
Altered mental status; increased confusion, decreased responsiveness, irritability, change in personality Decreased speech, sensation and movement Changes in vision Vomiting Fever, chills Neck stiffness Photophobia
246
Investigations to diagnose brain abscess?
MRI/ CT scan Ultrasound scan in infants Bloods; FBC, U+E, CRP, LFT, glucose
247
When can ultrasound be used to image brain?
When fontanelles are open
248
What is seen on imagining in brain abscess?
One or more ring enhancing lesion
249
Differentials for brain abscess?
Primary CNS neoplasm Metastatic lesion Recurrent tumour/ irradiation necrosis Multiple sclerosis Acute disseminated encephalomyelitis Ischaemic stroke
250
Management of brain abscess?
Antibiotics; vancomycin, metronidazole/ clindamycin, ceftriaxone Supportive care; corticosteroids, anticonvulsants, monitor vitals, surgical evacuation
251
Monitoring requirements for brain abscess?
Periodic CT with contrast until lesion have resolved, minimum for 1 year
252
Complications of brain abscess?
Ventriculitis Hyponatraemia Cognitive dysfunction Seizures Death Hydrocephalus
253
Prognosis of brain abscess?
Mortality of 10% Major factor is patients neurological status upon presentation Early diagnosis and treatment improves outcome
254
What is Guillain-Barre syndrome?
Acute inflammatory demyelinating ascending polyneuropathy against Schwann cells of peripheral sensory and motor nerves
255
What are the defining features of GBS?
Motor difficulty Absence of deep tendon reflexes Paraesthesia without objective sensory loss Increased CSF albumin with normal cell count
256
Epidemiology of GBS?
Most common acute polyneuropathy More common in men Associated with infection
257
Aetiology of GBS?
Campylobacter jejuni Cytomegalovirus Mycoplasma Zoster HIV EBV
258
Pathophysiology of GBS?
Auto-immune reaction Molecular mimicry where antibodies or T cells stimulated in response to pathogenic antigen epitopes cross react with neural epitopes Results in immune mediated damage to neural schwann cells resulting in reduced peripheral nerve conduction
259
Risk factors for GBS?
Preceding viral or bacterial infection Mosquito bites Hepatitis E Immunisation Cancer Male
260
Clinical presentation of GBS?
1-3 weeks post infection Symmetrical ascending muscle weakness ( proximal muscles affected more; trunk, respiratory, cranial nerve) Back and leg pain Respiratory weakness/ distress Speech problems, diplopia Areflexia, hyporeflexia, absent deep tendon reflexes Facial/ extra-ocular muscle weakness Pupillary dysfunction
261
Investigations to diagnose GBS?
Nerve conduction studies Lumbar puncture Spirometry/ LFT
262
What is seen on nerve conduction studies in GBS?
Prolonged distal and F-wave latency Reduced conduction velocity H reflex prolonged/ absent
263
Differentials for GBS?
Transverse myelitis  Myasthenia gravis Lambert- eaton myastenic syndrome Botulism Polymyositis Vasculitic neuropathy
264
Management of GBS?
Without IgA deficiency or renal failure; IVIG, supportive therapy, plasma exchange With lgA deficiency or renal failure, plasma exchange, supportive treatment
265
Monitoring requirements in GBS?
Follow-up within 2 weeks of acute syndrome  Every 4-6 weeks for 6 months  Followed by annual follow ups  Access to physiotherapy, occupational therapy and psychological support
266
Complications of GBS?
Respiratory failure Bladder areflexia Adynamic ileus Paralysis Fatigue DVT Immobilisation hypercalcaemia
267
Factors predicting poorer prognosis in GBS?
Severe weakness Rapid onset Older age Muscle wasting Electrically inexcitable nerves Preceding diarrhoeal illness
268
What in epilepsy?
Recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain manifesting in seizures Disease of brain with atleast two unprovoked seizures occuring more than 24 hours apart
269
What is an epileptic seizure?
Paroxysmal/ unprovoked event in which changes of behaviour, sensation or cognitive processes are caused by excessive, hypersynchronous neuronal discharge
270
What is the epidemiology of epilepsy?
Incidence is age dependent; highest before 20 years and after 60 years Focal seizures are most common
271
What is the cause of generalised epilepsies?
Unprovoked Provoked; toxins, illicit substance, medications, metabolic derangement and mutations in genes coding for ion channels
272
What is the cause of focal epilepsy?
Traumatic brain injury CNS infection Brain tumour and space occupying lesions Stroke Alzehimer's Perinatal injury Alcohol withdrawal Malformation in cortical development
273
Pathophysiology of epilepsy?
Inappropriate hyperexcitability and hypersynchrony Neurones have abnormal capability to generate intrinsic discharge bursts with decreased GABA inhibition and activation of local excitatory currents Genetic and structural abnormality contribute to neurones behaving in this manner
274
What are the elements of a seizure?
Prodrome Aura Ictal Post- ictal
275
What happens during seizure prodrome?
Lasts hours/ days Not part of the seizure Results in change in mood and behaviour
276
What happens during seizure aura?
Strange feeling in gut, deja vu, strange smells, and visual changes Patient is aware of symptoms and can feel seizure coming
277
What happens during ictal stage?
The seizure; presentation depends on type of seizure
278
Risk factors for generalised epilepsy?
Family history Previous CNS infection Head trauma Substance abuse Premature birth Multiple or complicated febrile seizures
279
Risk factors for focal epilepsy?
Febrile seizure Traumatic brain injury CNS infection Stroke Brain tumour Intellectual disability Cerebral palsy Dementia Family history of seizures Intracranial vascular malformations Male sex
280
Presentation of generalised tonic clonic seizure?
Often no aura Loss of consciousness Tonic phase; rigid, stiff limbs, person will fall to the floor Clonic phase; generalised bilateral rhythmic muscle jerking lasting seconds to minutes Eyes remain open Tongue biting Urine and faecal incontinence Post ictal phase of drowsiness, confusion and muscle ache
281
Presentation of absence seizure?
Disorder of childhood Ceases activity, stares and pales for a few seconds Suddenly stops talking mid sentence Often does not realise this has happened EEG shows 3-Hz spike and wave activity Children tend to develop generalised tonic-clonic seizures in adult life
282
Presentation of myoclonic seizure?
Sudden isolated jerk of limb, face or trunk Patient may be thrown suddenly to the ground or violently disobedient limb
283
Presentation of tonic seizure?
Sudden sustained increased tone Characteristic cry/ grunt Stiffening not followed by jerking
284
Presentation of atonic seizure?
Sudden loss of muscle tone and cessation of movement Results in falling
285
What seizures are classed as generalised seizures?
Generalised tonic clonic Absence Myoclonic Tonic Atonic
286
Presentation of simple partial seizure?
Not affecting consciousness or memory Awareness if unimpaired with focal motor, sensory, autonomic or psychic symptoms No post-ictal symptoms
287
Presentation of complex partial seizure?
Affects awareness or memory before, during or after seizure Commonly arise from temporal lobe Post ictal confusion is common in those originating from temporal lobe Rapid recovery in those originating from frontal lobe
288
Investigations to diagnose epilepsy?
Bloods; FBC, U+E, LFT, TFT, glucose Lumbar puncture and CSF analysis; rule out infection CT/ MRI; identify anatomical abnormalities and space occupying lesion EEG
289
Differentials for epilepsy?
Syncope Transient ischaemic attack Parkinsons Meniere’s disease Panic attack Psychiatric illness
290
Management of generalised seizure?
Sodium valproate/ lamotrigine Carbamazepine If medications are not helpful consider surgery or vagal nerve stimulation
291
What other medication can be offered to treat absence seizures?
Ethosuximide
292
Monitoring requirements in epilepsy?
Patients on anticonvulsants should be monitored every 6-12 months Every 1-2 months if medication dose is altered Ask patients to keep seizure diaries Routine blood tests to monitor blood biochemistry
293
Complications of epilepsy?
Head trauma Bone fracture Memory loss Mood disorder Sudden unexpected death in epilepsy Status epilepticus
294
Prognosis of epilepsy?
Majority of patients achieve adequate seizure control If a single identifiable cause can be found, surgical treatment can offer 70% chance of seizure free
295
What is status epilepticus?
Neurological emergency Convulsive seizures that continue for a prolonged period of time with no recovery in between
296
Aetiology of status epilepticus?
Epilepsy Drug withdrawal Neurological insult or systemic abnormality Hypoxia, stroke Metabolic abnormality Alcohol intoxication or withdrawal
297
Pathophysiology of status epilepticus?
When seizure aborting mechanisms fail, excessive and normally persistent excitation or ineffective inhibition result in rapid and random neural firing. Accumulation of excitatory neurotransmitters leads to cerebral damage
298
Risk factors for status epilepticus?
Poor anticonvulsant therapy adherence Alcohol abuse Stroke Recreational drug use
299
Clinical presentation in status epilepticus?
Prolonged/ repeated tonic- clonic seizures with altered level of consciousness Confusion Change in personality
300
Differentials for status epilepticus?
Psychogenic non-epileptic status Delirium Coma
301
Management of status epilepticus?
ABCDE Supportive care; ECG, GCS, glucose Benzodiazepine rectal if no IV access Consider; levetiracetam, sodium valproate, phenytoin
302
Monitoring requirements for status epilepticus?
Neurological observations Standards observations NICE recommends regular anticonvulsant drug levels
303
Complications of status epilepticus?
Focal neurological deficit Cognitive dysfunction; notably memory deficits Behavioral problems
304
What is diabetic neuropathy?
Peripheral nerve dysfunctions with/ without autonomic nerve dysfunction as a complication of diabetes mellitus
305
Epidemiology of diabetic neuropathy?
Most common complication of diabetes mellitus
306
What is the most common type of diabetic neuropathy?
Chronic sensorimotor polyneuropathy Autonomic dysfunction
307
Causes of neuropathy?
Toxins; alcohol B12 deficiency Medication induced; metformin, proton pump therapy Chemotherapy Hypothyroidism Renal disease Malignancy Monoclonal gammopathy Infections Chronic inflammatory demyelinating neuropathy Vasculitis
308
Pathophysiology of diabetic neuropathy?
Metabolic and vascular factors result in low grade inflammation Impaired mitochondrial function mediates Schwann cell injury Progressive damage and loss of peripheral nerve fibres Results in impaired sensory function and sometimes autonomic dysfunction
309
Risk factors for diabetic neuropathy?
Duration of diabetes Poorly controlled hyperglycaemia Dyslipidaemia with elevated triglycerides Immune dysregulation Height Body mass index Age over 70 years
310
Clinical presentation of diabetic neuropathy?
Peripheral pain; prickling, burning, aching, worse at night Loss of peripheral sensation; proceeds proximally causing symmetrical distal sensory loss, glove and stocking pattern Painless foot injuries/ ulceration Dysaesthesia; abnormal sensation of burning, tingling and numbness Absent ankle reflexes Autonomic features
311
What autonomic features present with diabetic neuropathy?
Resting tachycardia Impaired heart rate variability Urinary frequency, urgency, nocturia incontinence, hesitancy, weak stream, retention Erectile dysfunction Decreased sexual desire Increased pain during intercourse Orthostatic hypotension
312
Investigations performed to diagnose diabetic neuropathy?
Clinical diagnosis HbA1c/ fasting glucose Routine baseline bloods Corneal confocal microscopy
313
Differentials for diabetic neuropathy?
Uraemia B12 deficiency Hypothyroidism Chronic raised alcohol intake Heavy metal poisoning Drug induced neuropathy Chronic inflammatory demyelinating neuropathy Cauda equina Myasthenia gravis
314
Management of diabetic neuropathy?
Improve glycaemic control Neuropathic pain management; pregabalin/ gabapentin, topical capsacin, TENS/ PENS
315
Monitoring requirements for diabetic neuropathy?
Foot screen and podiatry Fundoscopy HbA1c
316
Complications of diabetic neuropathy?
Foot wounds/ ulcers Wound infection/ gangrene Amputation Silent MI Death Depression Charcot foot
317
Prognosis of diabetic neuropathy?
Depends of glycaemic control Neuropathy is associated with increased mortality
318
What is an essential tremor?
Progressive tremor of the upper extremities in posture and action, without other neurological signs or symptoms
319
What does an essential tremor look like?
Symmetrical, rhythmic, involuntary, oscillation movement disorder of hands and forearm Usually absent at rest and present during posture and intentional movements
320
Epidemiology of essential tremor?
Most common movement disorders Incidence increases with age More common in white ancestry
321
Aetiology of essential tremor?
Ageing, genetics Environmental toxin exposure
322
Pathophysiology of essential tremor?
Involves cerebellum, brainstem and thalamus GABAnergic dysfunction of cerebellar dentate nucleus in brainstem due to neurodegeneration leads to tremulous activity within cerebellothalamocortical circuit resulting in involuntary movement of upper limb
323
Risk factors for essential tremor?
Advanced age Family history White ancestry Exposure to environmental toxins
324
Clinical presentation of essential tremor?
Postural/ kinetic tremor; bilateral upper limb action tremor with absence of other neurological signs Problems with fine motor tasks Medications suppress tremor
325
What medications suppress action tremor?
Alcohol, benzodiazepines, gabapentin, barbiturates
326
Investigations to diagnose essential tremor?
Clinical diagnosis from history EMG silence in all muscles groups except tremulous muscles CT/ MRI head to rule out other causes
326
Differentials for essential tremor
Parkinson's disease Dystonia Wilson's disease Enhanced physiological tremor Drug- induced tremor Psychogenic tremor Orthostatic tremor
327
Management of essentials tremor?
Watch and wait Medications; propanolol, primidone, gabapentin, alprazolam, topiramate Deep brain stimulation Gamma knife thalamotomy
328
Monitoring requirements for essential tremor?
Annual visits to monitor progression
329
Complications of essential tremor?
Deep brain stimulation related paraesthesia, dysarthria, gait disorder
330
Prognosis of essential tremor?
Persistent and progressive disorder Many patients are mildly affected Some can have social handicap and embarrassment No cure, but treatment to improve quality of life
331
Classification of tremor?
Essential tremor Rest tremor Action tremor Mixed action/ rest tremor
332
Causes of rest tremor?
Parkinson's disease Dementia with lewy bodies Multisystem atrophy Progressive supranuclear palsy Toxin induced parkinsonism; carbon disulphide, carbon monoxide, cyanide, manganese, herbicides, organic solvents
333
Causes of action tremor?
Enhanced physiological tremor Essential tremor Cerebral tremor; MS, trauma, stroke Fragile X tremor ataxia syndrome Orthostatic tremor Primary writing tremor Neuropathic tremor
334
Causes of mixed action/ resting tremor?
Drug induced tremor Dystonic tremor Tremor secondary to wilsons disease Psychogenic tremor Holmes tremor; Rubral, midbrain tremor
335
What is Parkinson's disease?
Chronic progressive neurodegenerative disorder characterised by presence of bradykinesia with resting tremor and/ or rigidity Reduced dopaminergic neurones in the substantia nigra
336
Epidemiology of Parkinson's disease?
Mean age of onset is 65 years Increasing prevalence with increasing age Rare condition Greater incidence in men More common in white people
337
Aetiology of Parkinson's disease?
Autosomal dominant and recessive forms of disease have been identified Mitochondrial dysfunction Environmental factors; chronic heavy metal exposure, oxidative damage by free radicals, pesticides, MTP
338
Pathophysiology of Parkinsons disease?
Degeneration of dopaminergic neurones in pars compacta of substantia nigra as a result of mitochondrial dysfunction and oxidative stress Reduced striatal dopamine resulting in inhibition of thalamus hence bradykinesia
339
How is Parkinson's classified?
According to age of onset; juvenile (under 21 years), Young onset (between 21 and 40 years)
340
Risk factors for Parkinson's?
Increasing age Family history Mutations in glucocerebrosidase gene MPTP exposure Male sex Head injury Occupational
341
Classic triad for Parkinsons?
Bradykinesia, Resting tremor, Cogwheel rigidity
342
Clinical presentation of Parkinsons?
Asymmetrical presentation Bradykinesia Resting tremor Rigidity Parkinsonian gait Postural instability Marked facies Hypophonia, drooling, swallowing difficulty Fatigue, dementia, sleep disorder Dementia Urinary problems
343
Investigations to diagnose Parkinsons?
Clinical based on history and examination  Dopaminergic agent trial; Symptoms Improve MRI head; Brain atrophy, Lewy bodies in late disease
344
Differentials of parkinsons?
Essential tremor Dementia Drug induced parkinsonism Metabolic abnormalities Corticobasal degeneration
345
Management of Parkinsons?
Non medical management; physiotherapy, occupational therapy, speech therapy, psychiatric management Medical management; Levodopa+decarboxylase inhibitor, dopamine antagonist, MAO-B/ COMT inhibitors
346
Monitoring requirements for Parkinson's disease?
Serial monitoring of movement disorder History and neurological examination to monitor progression
347
Complications of Parkinson's?
Levodopa induced dyskinesia Motor fluctuations Dementia Constipation, bladder dysfunction Depression, psychosis, anxiety
348
Prognosis of Parkinsons?
No curative or disease modifying agents Factors favoring poorer prognosis; older age of symptoms, rigidity hypokinesia, reduced response to dopaminergic medications
349
What is Huntington's disease?
Autosomal dominant neurodegenerative disorder characterised by chorea, incoordination, cognitive decline, personality change and psychiatric symptoms
350
Epidemiology of Huntington's disease?
20 years from diagnosis to death Affects men and women equally Onset between 35 and 45 years More common in North American and European ancestry
351
Aetiology of Huntington's disease?
Expanded CAG repeats at N-terminus of gene coding for huntingtin protein
352
How many CAG repeats are needed to develop Huntington's?
40 or more
353
Which parent is more likely to pass on Huntington's?
Father as pathogenic trinucleotide repeat is less stable in spermatogenesis
354
Pathophysiology of Huntington's?
CAG repeat produces elongated polyglutamine tail on huntingtin protein leading to cleavage and generation of toxic fragments of abnormal protein , predisposing cross linking and aggregation resistant to deformation Aggregates interfere with normal cellular function, mitochondrial metabolism, apoptosis, proteosome function
355
Which region of brain is most affected by Huntington's?
Striatum
356
Risk factors for Huntington's?
Family history European, North American ancestry
357
Clinical presentation of Huntington's?
Chorea Personality change Impaired performance at work/ school Impulsivity Twitching/ restlessness Milk maids grip Saccadic eye movements Loss of coordination
358
Describe Huntington's chorea?
Continuous flow of jerky, semi purposeful movements Occasional peculiar postures of hands, trunk or limbs and odd facial expressions
359
Investigations to diagnose Huntington's?
Clinical diagnosis CAG repeat genetic testing MRI or CT scan
360
Differentials for Huntington's?
Tardive dyskinesia Benign hereditary chorea Hyperthyroid chorea Wilson's disease Lupus cerebritis Antiphospholipid antibody syndrome
361
Management of Huntington's?
No disease modifying treatment Chorea; benzodiazepines, sulphide, tetrabenazine Antidepressants, antipsychotics Aggression; risperidone
362
Monitoring requirements for Huntington's?
Every 6-12 months Aim to review symptom, identify cover fatigue
363
Complications of Huntington's?
Weight Ioss Dysphagia Falls Suicide risk Incontinence
364
Prognosis of Huntington's?
Duration of disease is 20 years from diagnosis to death
365
What is normal pressure hydrocephalus?
Clinical features of hydrocephalus without significantly raised CSF pressure
366
Aetiology of normal pressure hydrocephalus?
Abnormal absorption of CSF Build up of toxic metabolites in CSF Abnormal arterial pulsatility compressing venous vasculature
367
Pathophysiology of normal pressure hydrocephalus?
Imbalance between CSF production and drainage through arachnoid granulations, either through scarring or obstruction
368
Risk factors for normal pressure hydrocephalus?
Age over 65 years Vascular disease Diabetes mellitus
369
Clinical presentation of normal pressure hydrocephalus?
Gait apraxia Cognitive impairment; mental slowing, memory impairment Urinary frequency/ incontinence/ urgency
370
Describe features of gait disturbance in normal pressure hydrocephalus?
Unresponsive to levodopa Slow, cautious, unsteady gait Reduced stride length Insidious onset Symmetrical Predominantly affects lower body
371
Investigations performed in normal pressure hydrocephalus?
CT/ MRI; enlarged ventricles, periventricular leukomalacia, cerebral infarction Levodopa challenge; No response Lumbar puncture; assess CSF properties, look for improvement in symptoms Continuous intracranial pressure monitoring
372
Differentials for normal pressure hydrocephalus?
Parkinson's disease Alzheimer's Other dementia Urinary outflow obstruction
373
Management of normal pressure hydrocephalus?
Surgical options; ventriculoperitoneal shunt, endoscopic third ventriculostomy Serial CSF tap
374
Monitoring requirements of normal pressure hydrocephalus?
Post operative monitoring for shunt function and infection
375
Complications of normal pressure hydrocephalus?
Stroke Subdural haematoma Bleeding Shunt infection Vascular disease Cognitive impairment
376
Prognosis of normal pressure hydrocephalus?
Extensive radiological change on neuroimaging Gait is most improved symptom and urinary symptoms show least improvement
377
What is Wernicke's encephalopathy?
Neurological emergency with varied neurocognitive manifestations including change in mental status, gait and oculomotor disturbance
378
Epidemiology of Wernicke's encephalopathy?
Prevalence between 0.8 and 2.8% More common in alcoholics and people with AIDS More prevalent in men
379
Aetiology of Wernicke's encephalopathy?
Acute or subacute thiamine deficiency as a result of decreased intake, relative deficiency compared to increased demand, malabsorption from GI tract
380
Pathophysiology of Wernicke's encephalopathy?
Thiamine deficiency leads to reduced activity of pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase Energy compromise leads to neuronal death Can affect memory circuits leading to Korsakoff's psychosis
381
Risk factors for Wernicke's encephalopathy?
Exclusive breast feeding Alcoholism AIDS Malnutrition of any cause; malignancy, gastric bypass surgery, haemodialysis, hyperemesis gravidarum Bone marrow transplantation Gastrointestinal surgery Genetic susceptibility Male sex
382
Clinical presentation of Wernicke's encephalopathy?
Mental slowing, impaired concentration and apathy Frank confusion Oculomotor disturbance; gaze palsies, sixth nerve palsy, impaired vestibular ocular reflex Change in mental status Opthalmoplegia Gait disturbance
383
Investigations to diagnose Wernicke's encephalopathy?
Finger prick glucose and screening full set of bloods Thiamine level
384
Differentials of Wernicke's encephalopathy?
Alcohol intoxication/ withdrawal Viral encephalitis Miller- Fisher syndrome Bickerstaff brainstem encephalitis Primary CNS lymphoma Toxic/ metabolic encephalopathies
385
Management of Wernicke's encephalopathy?
ABCDE management Thiamine, magnesium, folic acid and multivitamin supplementation
386
Monitoring requirements for Wernicke's encephalopathy?
Neurocognitive evaluation for residual deficits Work appropriate neuropsychological evaluation Patients should be followed periodically to ensure they do not relapse and are adherent to supplementation
387
Complications of Wernicke's encephalopathy?
Ataxia Varying degree of ophthalmoparesis Korsakoff’s psychosis Hearing loss Seizures Spastic paraparesis
388
Prognosis of Wernicke's encephalopathy?
If not recognised and treated can cause permanent brain injury with impairment in recent and remote memory, apathy and confusion
389
What is Bell's palsy?
Acute unilateral peripheral facial nerve palsy with deficits affecting all facial zones
390
What is Ramsy- Hunt syndrome?
Specific form of facial nerve palsy caused by varicella zoster infection
391
Epidemiology of Bell's palsy?
Most common cause of facial nerve palsy No dominant gender or side of face affected Common between 15 and 45 years of age
392
Aetiology of Bell's palsy?
Reactivation of HSV-1 Inflammation and immune response
393
Pathophysiology of Bell's palsy?
Reactivation of HSV-1 destroys ganglion cells and infection of Schwann cells leads to demyelination and neural inflammation causing oedema in exit canal of CN8 compression the nerve and causing transient ischaemia and nerve dysfunction
394
Risk factors for Bell's palsy?
Intranasal influenza vaccination Pregnancy Upper respiratory tract infection Arid/ cold climate Hypertension Family history of Bell’s palsy Diabetes Dental procedures
395
Clinical presentation of Bell's palsy?
Unilateral facial muscle weakness Keratoconjunctivitis sicca Post auricular pain with mild to moderate otalgia Facial synkinesis
396
Investigations to diagnose Bell's palsy?
Clinical diagnosis from hsitory EMG
397
Differentials for Bell's palsy?
Ramsay hunt syndrome Lyme disease Benign/ malignant facial nerve tumour Chronic otitis media
398
Treatment for Bell's palsy?
Prednisolone within 72 hours of symptom onset Eye drops If severe disease then decompression surgery and antiviral therapy may be needed
399
Monitoring requirements for Bell's palsy?
1-2 weeks following initial visit Then monthly or 3-monthly follow-up to monitor recovery
400
Complications associated with Bell's palsy?
Keratoconjunctivitis sicca Ectropion (eyelid sagging) Contracture and synkinesis Gustatory hyperlacrimation
401
Prognosis of Bell's palsy?
Majority make full recovery Poorer prognostic factors; advancing age, diabetes mellitus, taste disturbance on presentation
402
What is Meniere's disease?
Episodic auditory/ vestibular disease characterised by sudden onset vertigo, low frequency hearing loss, low frequency tinnitus and sudden sensation of fullness in ear
403
Epidemiology of Meniere's disease?
Affects adults, typically in 4th decade Slight female predominance
404
Aetiology of Meniere's disease?
Idiopathic Allergies Congenital or acquired syphilis, lyme disease Hypothyroidism Stenosis of internal auditory canal
405
Pathophysiology of Meniere's disease?
Impaired endolymph absorption forms endolymphatic hydrops increasing endolymphatic fluid pressure leading to reupture of Reissner's membrane This releases K+ rich endolymph into peri-lymphatic space injuring sensory and neural elements In between attacks membrane may reattach and symptoms remit
406
Risk factors for Meniere's disease?
Viral infection Genetic pre-disposition; autosomal dominant, X-linked Autoimmune disease
407
Clinical presentation of Meniere's disease?
Vertigo Hearing loss Tinnitus Aural fullness
408
Investigations to diagnose Meniere's disease?
Positive romberg's test Pure- tone air and bone conduction with masking; Unilateral sensorineural hearing loss Speech audiometry Tympanometry/ immittance/ stapedial reflex levels Oto-acoustic emissions
409
Differentials for Meniere's disease?
Acoustic neuroma Vestibular migraine Vestibular neuronitis Viral labyrinthitis Benign paroxysmal positional vertigo Vertebrobasilar insufficiency
410
Acute management for Meniere's disease?
Thiazide diuretic +/- K+ sparring diuretic Vertigo; anti-emetic, corticosteroid, vestibular suppressant Tinnitus; benzodiazepine
411
Long term management for Meniere's disease?
Dietary and lifestyle change Hearing aid Endolymphatic sac surgery, vestibular nerve resection, labyrinthectomy
412
Monitoring requirements for Meniere's disease?
Follow- up with audiologist and otologist Regular hearing tests and monitor symptoms
413
Complications of Meniere's disease?
Falls Profound hearing loss
414
Prognosis of Horner's syndrome?
Symptoms worsen regardless of interventions Unpredictable course, may have periods of remission
415
What is Horner's syndrome?
Compression of sympathetic trunk presenting with ptosis, miosis, anhidrosis
416
Epidemiology of Horner's syndrome?
Uncommon, occuring 1 in 6000 No gender, age or ethnicity predominance
417
Aetiology of Horner's syndrome?
First order neurons; stroke, tumour, demyelinating disease, neck trauma, cyst in spinal cord Second order neuron; lung cancer, schwannoma, damage to aorta, surgery in chest cavity, traumatic injury Third order neurons; damage to carotid/ jugular, tumour or infection near base of skull, migraines
418
Pathophysiology of Horner's syndrome?
Compression of sympathetic chain
419
Clinical presentation of Horner's syndrome?
Classic triad; anhidrosis, miosis, ptosis Notable difference in size of pupil Delayed dilation of pupil in dim light Slight elevation of lower lid Sunken appearance in affected eye
420
Investigations to diagnose Horner's syndrome?
Look for cause of compression; CXR, CT, MRI, angiography
421
Differentials for Horner's syndrome?
Carotid artery dissection Neuroblastoma Neurosyphilis
422
Management of Horner's syndrome?
Treat the cause of compression No particular treatment for Horner's syndrome
423
Complications/ prognosis of Horner's syndrome?
Depends on aetiology
424
What is neurofibromatosis?
Autosomal dominant genetic disorder with characteristic features; cafe au lait spots, multiple neurofibroma, irish lisch nodules
425
What are the classic features of NF?
Café au lait spots Multiple neurofibroma Irish Lisch nodules
426
Epidemiology of NF?
Autosomal dominant mutation
427
Where is the genetic mutation in NF1?
NF 1 gene on chromosome 17
428
Pathophysiology of Neurofibromatosis 1?
Reduction in NF1 gene product neurofibromin which is a tumour suppressor protein, disrupts Ras-oncogene mediated signaling in Schwann cells, glia, melanocytes and other cells derived from ectoderm Tissue specific dysplasia/ neoplasia
429
Risk factors for neurofibromatosis?
Parent with NF Severe crush trauma
430
Clinical presentation of NF?
Pain in any location; usually due to peripheral neurofibroma Neurological deficit; gross motor delay, incoordination, performance problems Skin changes; cafe au lait spits, axillary freckling, cutaneous neurofibroma Visual change; optic disk pallor, irish lisch nodules, visual compramise CNS signs; hydrocephalus, cerebellar abnormalities PNS signs; palpable mass in neck, brachial plexus, groin, popliteal fossa Skeletal signs; tibial dysplasia, pseudoarthrosis, sphenoid wing dysplasia Gastrointestinal; constipation, abdominal pain, gastrointestinal bleeding
431
Investigations to diagnose NF?
MRI/ CT/ PET scan; look for tumours, hydrocephalus Biopsy Genetic test to confirm NF1 mutation
432
Differentials for NF?
Neurofibromatosis type 2 McCune-Albright syndrome Familial cafe au lait spots Age related cutaneous neurofibromas Schwannomatosis
433
Management of NF?
Surgical removal of tumours Physiotherapy, psychological therapy Frequent follow-up
434
Monitoring requirements for NF?
Annual review including history, physical exam of eyes, nervous system, skeleton, skin and CVS Women offered mammogram from 30 years
435
Complications of NF?
Migraine Epilepsy Renal artery stenosis causing hypertension Learning and behavioural problems Scoliosis of spine Vision loss Malignant peripheral sheath tumours Gastrointestinal stromal tumour Spinal cord tumour Breast cancer Leukaemia
436
Prognosis of NF?
Reduced life-expectancy due to cardiovascular complications and malignancy
437
What is the cause of NF 2?
Mutation on chromosome 22 coding for protein merlin (tumour suppressor protein)
438
Which cells does NF2 affect more?
Schwann cells
439
What is the inheritance pattern of NF2?
Autosomal dominant
440
What type of NF is associated with acoustic neuroma?
NF 2
441
What sign is indicative of NF2?
Bilateral acoustic neuroma
442
What is acoustic neuroma?
Benign cerebellopontine angle tumour
443
Epidemiology of acoustic neuroma?
Female predominance
444
Aetiology of acoustic neuroma?
Sporadic Neurofibromatosis type 2
445
Pathophysiology of acoustic neuroma?
Benign growth at cerebello- pontine angle causing compression of vestibulocochlear nerve producing problems with hearing and balance
446
Risk factors for acoustic neuroma?
NF type 2
447
Clinical presentation of acoustic neuroma?
Unilateral sensorineuronal hearing loss, tinnitus Dizziness, imbalance Fullness in inner ear If bilateral think of NF type 2
448
Investigations to diagnose acoustic neuroma?
Audiometry; sensorineural pattern hearing loss Auditory brainstem reflexes MRI/ CT; look for tumour
449
Differentials for acoustic neuroma?
Meningioma Facial/ trigeminal nerve schwannoma
450
Management of acoustic neuroma?
Conservative monitoring if not surgical candidate Surgery to remove tumour Radiotherapy
451
Monitoring requirements of acoustic neuroma?
MRI every 6 months to monitor growth, then yearly when stable After surgery a baseline MRI and one after a few months, then annually for 5 years
452
Complications of acoustic neuroma?
Surgical complications; injury to vestibulocochlear nerve, facial weakness/ paraesthesia, CSF fluid leak Radiation complications; Hydrocephalus, secondary malignancy, hearing loss, facial nerve palsy
453
Prognosis of acoustic neuroma?
Good prognosis with minimal complications 40-60% of tumours do not require treatment
454
What is cauda equina syndrome?
Compression of lumbosacral nerve roots that extend below spinal cord
455
Epidemiology of cauda equina syndrome?
1-2 cases per 100,000 Equal incidence between race, gender Under 50 more likely to have acute presentation, over 50 more progressive
456
Aetiology of cauda equina syndrome?
Disk herniation at L4/L5 Spinal stenosis Traumatic injury Spinal tumour Epidural haematoma, abscess
457
Most common cause of cauda equina syndrome?
Disk herniation
458
Pathophysiology of cauda equina syndrome?
Bundle of spinal nerves L1- S5 which innervate bladder, bowel, lower limb muscle and sexual function Compression of these nerve roots produces symptoms
459
Classification of cauda equina syndrome?
Incomplete; thecal sac compression with no urinary retention Complete; thecal sac compression with established neurogenic urinary retention
460
Risk factors for cauda equina syndrome?
Lumbar disk herniation Spinal trauma Spinal surgery Spinal epidural abscess Anticoagulation therapy; increases risk of haematoma Spinal stenosis Spinal tumour
461
Clinical presentation of cauda equina syndrome?
Lower limb weakness Saddle paraesthesia/ anaesthesia Bowel dysfunction Bladder dysfunction and retention Lower back pain Sciatica Sexual dysfunction
462
Investigations to diagnose cauda equina syndrome?
CT/ MRI; visualise compression Urodynamic testing
463
Differentials for cauda equina syndrome?
Spinal epidural abscess Osteoporotic spinal compression fracture Transverse myelitis GBS Traumatic conus medullaris
464
Management of cauda equina syndrome?
Decompression surgery Bladder and bowel management `
465
Monitoring requirements in cauda equina syndrome?
Long term bladder, bowel, sexual and physical dysfunction monitoring Physiotherapy
466
Complications of cauda equina syndrome?
Bladder dysfunction Bowel dysfunction Sexual dysfunction Sensory impairment Leg weakness
467
Prognosis of cauda equina syndrome?
Degree of neurological dysfunction at surgery indicates prognosis Poorer prognostic factors; urinary retention, delay of surgery
468
What is chronic spinal cord injury?
Symptoms of spinal cord injury that have been present for at least 12 months resulting in permanent/ progressive interruption in conduction of impulses across neurons and tracts of spinal cord
469
Epidemiology of chronic spinal cord injury?
75% of patients are male Children and elderly are most at risk Falls are most common cause?
470
Why are children and elderly at highest risk of chronic spinal cord injury?
Less developed neck musculature Horizontal orientation of facets Relative ligamentous laxity
471
Aetiology of chronic spinal cord injury?
Traumatic; compression from haematoma, dissection/ shearing/ laceration trauma Non traumatic injury; degeneration, compression from tumours, infection Congenital narrowing of spinal column Vascular injury
472
Pathophysiology of chronic spinal cord injury?
Inflammatory response secondary to initiating factor resulting in disability and depends on which region of the spinal cord is affected
473
Risk factors for chronic spinal cord injury?
Spinal cord trauma or ischaemia Extremes of age Narrow spinal canal Male sex
474
Clinical presentation of chronic spinal cord injury?
Motor weakness Loss of fine motor coordination Spasticity Paraesthesia, numbness, dysaesthesia Hyperreflexia and ankle clonus Autonomic dysreflexia
475
Signs of autonomic dysreflexia?
Sudden uncontrolled rise in blood pressure Pounding headache Sweating Shivering Anxiety Chest tightness Blurred vision
476
Investigations to diagnose chronic spinal cord injury?
MRI; look for lesions, spinal column abnormalities EMG; localise neuromuscular pathology Urodynamic studies
477
Differentials for chronic spinal cord injury?
Compressive myelopathy Non compressive myelopathy
478
Management of chronic spinal cord injury?
If compressive; surgical decompression in timely manner and vasodilatory therapy if autonomic dysreflexia Rehabilitation, pain control, physiotherapy, spasticity management
479
Monitoring requirements in chronic spinal cord injury?
VTE prophylaxis If on opiates monitor respiratory drive
480
Complications of chronic spinal cord injury?
Disturbance in bowel and bladder control Respiratory dysfunction Sexual dysfunction Joint contractures Neuropathic pain Autonomic dysreflexia
481
Prognosis of chronic spinal cord injury?
Depends on severity of neurological deficit Decreased life expectancy
482
What is Narcolepsy?
Chronic sleep disorder affecting control of sleep and wakefulness with REM sleep intrusion into wake state
483
Characteristic of narcolepsy?
Excessive daytime sleepiness Cataplexy; generalised muscle weakness leading to partial or complete collapse Hypnagogic/ hypnopompic hallucinations; visual or auditory perceptions on falling asleep or awakening Sleep paralysis
484
Epidemiology of narcolepsy?
2 per 1000 cases Second most common cause of disabling daytime sleepiness after obstructive sleep apnoea
485
Aetiology of narcolepsy?
Head trauma Stroke Brain or hypothalamic tumours CNS infection/ inflammation Arteriovenous malformations Multiple sclerosis Paraneoplastic anti-Ma antibodies Niemann-Pick disease type C, Norrie’s disease, Prader-Willi syndrome
486
Risk factors for narcolepsy?
HLA-2 DQA1, DQB2 Prader-Willi syndrome Low CSF hypocretin Hypothalamic tumours, infarct, haemorrhage
487
Investigations to diagnose narcolepsy?
Actigraphy and sleep diary Overnight polysomnography Multiple sleep latency tests
488
Differentials for narcolepsy?
Obstructive sleep apnoea Periodic limb movement of limbs Restless leg syndrome Behaviourally induced insufficient sleep syndrome Hypersomnia due to medications/ psychiatric conditions Idiopathic hypersomnia Menstrual related hypersomnia
489
Management of narcolepsy?
Regular and adequate amounts of sleep during night Schedule naps to optimise daily function Avoid heavy meals and afternoon caffeine/ alcohol Medications; Modafinil, pitolisant, sodium oxalate
490
Monitoring requirements in narcolepsy?
Follow up every 6-12 months to re-evaluate social support, symptoms and medications
491
Complications of narcolepsy?
Traffic accidents Depression
492
Prognosis of narcolepsy?
Lifelong condition Almost half patients have daily impairment from symptoms
493
What is myalgic encephalomyelitis?
Chronic fatigue syndrome for more than 6 months, with combination of cognitive dysfunction, total body pain, unrefreshing sleep, post exertional malaise
494
Epidemiology of myalgic encephalomyelitis?
Peak onset between 30 and 50 years 2-3 times more common in women More common in ethnic minority groups
495
Aetiology of myalgic encephalomyelitis?
Post COVID syndrome Viral and bacterial infections; EBV, mycoplasma pneumonia Neuroendocrine Genetic Gastrointestinal Psychological IgG subclass deficiencies
496
Risk factors of myalgic encephalomyelitis?
Female sex EBV infection in adolescents COVID Family history Genetic factors Autoimmune disease Gut microbiome
497
Clinical presentation of myalgic encephalomyelitis?
Persistent disabling fatigue for over 6 months Post exertional malaise Short term memory/ concentration impairment Sore throat Generalised arthralgia without inflammation Unrefreshing sleep Orthostatic intolerance
498
Investigations to diagnose myalgic encephalomyelitis?
DePaul symptom questionnaire/ clinical diagnosis FBC with WCC differential, CRP, ESR, comprehensive metabolic panel, TSH, anti- ANA, anti- RF HIV antibody test
499
Differentials for myalgic encephalomyelitis?
COVID Migraine Anxiety Major depressive episode Sleep apnoea Fibromyalgia Reaction to life crisis Dehydration Psychiatric illness
500
Management of myalgic encephalomyelitis?
No curative treatment, treat the symptoms and improve functional capacity Occupational therapy, physical therapy CBT and psychiatry referral
501
Monitoring requirements for myalgic encephalomyelitis?
Management with single primary care physician See patient every 3 months to counsel and reassess situation and symptoms
502
Complications of myalgic encephalomyelitis?
Major depressive episode
503
Prognosis of myalgic encephalomyelitis?
Lifelong condition with symptom management as there is no treatment
504
What are the types of MND?
Amyotrophic lateral sclerosis Primary lateral sclerosis Progressive muscular dystrophy Progressive bulbar palsy
505
What is ALS?
Neurogenerative disorder characterised by progressive muscle weakness that can start in any limb, axial, bulbar or respiratory muscles and then become generalised causing progressive disability
506
Epidemiology of ALS?
Mean age of onset is 62 years Peak incidence between 60 and 75 years More common in men Higher incidence in white ethnicity
507
Aetiology of ALS?
Sporadic
508
Pathophysiology of ALS?
Progressive loss of cortical, bulbar and ventral cord motor neurons After motor cell death retrograde axonal degeneration followed by denervation and reinnervation in corresponding muscles Glutamate toxicity, protein misfolding, oxidative stress, inflammation, mitochondrial dysfunction are involved in pathophysiological changes
509
Risk factors for ALS?
Genetic/ family history Age over 40 years Military service Professional athletic activity Smoking Agricultural chemical exposure Lead exposure
510
Clinical presentation of ALS?
UMN symptoms Upper extremity weakness; Difficulty in performing ADL Stiffness with poor coordination and balance Stiffness and decreased balance with impact on gait; UMN truncal weakness Hyperreflexia Dyspnoea Strained slow speech Hypophonic speech LMN symptoms Spasticity and unsteady gait Painful muscle spasm Difficulty arising from chair or going up stairs Foot drop Head drop; LMN axial weakness Difficulty maintaining erect posture Muscle atrophy
511
Investigations to diagnose ALS?
Clinical presentation and history Neuroimaging and bloods to rule out other causes
512
Differentials for ALS?
Cervical spondylosis with myelopathy and radiculopathy Inclusion body myositis Monomelic amyotrophy Myasthenia gravis Post- polio syndrome Other types of motor neurone disease
513
Management for ALS?
Riluzole at diagnosis Respiratory symptoms; Non invasive ventilation Dysphagia and weight loss; diet modification, feeding tube Dysarthria; alternative communication methods Muscle weakness; physiotherapy Spasticity; physiotherapy, baclofen, tizanidine, botox Psychiatric management
514
Which medication is prognostic in ALS?
Riluzole
515
Monitoring requirements for patients taking riluzole?
LFT and FBC every 3 months due to risk of neutropenia and hepatotoxicity
516
Monitoring requirements in ALS?
Respiratory function and nutritional status every 3 months Bloods every 3 months if on riluzole
517
Complications of ALS?
Respiratory failure Nutritional deficit Aspiration pneumonia Riluzole related hepatotoxicity/ neutropenia
518
Poorer Prognostic factors for ALS?
Older age at diagnosis Bulbar onset Comorbid frontotemporal dementia Baseline FVC below 75% Substantial weight loss
519
Good prognostic factors for ALS?
Treatment with non-invasive ventilation Enteral nutrition Younger age at diagnosis Limb onset Line first vital capacity over 75% Longer time from symptom onset to diagnosis
520
Prognosis of ALS?
Mean survival is 3-5 years from diagnosis Progressive illness
521
What is brown sequard syndrome?
Lesion of spinal cord resulting in weakness/ paralysis, sensory distrubance on the same side as lesion and contralateral pain and temperature sensory disturbance due to hemisection of the spinal cord
522
Epidemiology of brown sequard syndrome?
Accounts for 4% of spinal cord injuries Most common cause is trauma
523
Aetiology of brown sequard syndrome?
Trauma; puncture, wound, penetrating trauma, gunshot wound, motor accident Ischaemia/ infarction/ haemorrhage Infectious disease Inflammatory disease Spinal cord tumour
524
Pathophysiology of brown sequard syndrome?
Clean cut hemi-section of spinal cord
525
Risk factors for brown sequard syndrome?
Penetrating trauma Infection
526
Clinical presentation of brown sequard syndrome?
Loss of voluntary function on same side of body below lesion Loss of pain and temperature sensation on contralateral body side below level of injury Incontinence
527
Investigations to diagnose brown sequard?
Clinical diagnosis Neuroimaging
528
Differentials for Brown sequard?
Stroke/ tumour/ cyst causing spinal cord compression Cauda equina syndrome
529
Management of brown sequard syndrome?
Decompressive surgery VTE prophylaxis Breathing support Rehabilitation; maintain strength and range of motion, improve mobility
530
Monitoring requirements in brown sequard syndrome?
Rehabilitation and physiotherapy involvement Monitor healing of injury
531
Complications of brown sequard syndrome?
Abdominal distention Depression Hypotension Pulmonary embolism Infection Permanent paralysis
532
Prognosis of brown sequard?
Depends of cause and degree of spinal cord injury
533
What is mononeuropathy?
Damage to single nerve lying close to skin or bone resulting in pain, loss of movement and sensation
534
Which nerves are commonly affected by mononeuropathy?
Median nerve; carpal tunnel syndrome Ulnar nerve; elbow Radial nerve; upper arm Peroneal nerve; below knee Lateral femoral cutaneous nerve; in the leg
535
What is the difference between mononeuropathy and radiculopathy?
Radiculopathy affects nerves as they leave the spinal canal and typically affects nerve roots Mononeuropathy affects peripheral nerves that lye close to skin and bone
536
Epidemiology of mononeuropathy?
Carpal tunnel syndrome is the most common form of entrapment neuropathy
537
Aetiology of mononeuropathy?
Poorly fitted casts/ crutches Pressure from staying fixed in a position for a long time/ paralysis Injury from radiation therapy
538
Pathophysiology of mononeuropathy?
Stiffness of soft tissue or pressure from underlying bone damages peripheral nerve causing impingement and nerve dysfunction
539
Risk factors for mononeuropathy?
Obesity Diabetes Pregnancy
540
Clinical presentation of mononeuropathy?
Loss of sensation in affected area Weakness in affected area Pain or burning Feelings of pins and needles
541
Investigations to diagnose mononeuropathy?
Clinical diagnosis from history Electromyography and nerve conduction studies Neuromuscular ultrasound and MRI imaging
542
Differentials for mononeuropathy?
Radiculopathy Chronic pain syndrome Alcoholic neuropathy Brachial neuritis GBS Acute compartment syndrome
543
Management of mononeuropathy?
Decompression surgery Corticosteroid injections Splints to immobilise the area
544
Complications of mononeuropathy?
Permanent weakness Impaired dexterity Permanent disability Loss of sensation Pain
545
Prognosis of mononeuropathy?
If caught and treated early then improved prognosis
546
What is radiculopathy?
Injury/ damage to nerve roots at the region the leave the spine
547
Aetiology of radiculopathy?
Degeneration wear and tear Arthritis Herniated discs Spondylosis Degenerative spondyloarthropathies Bone spurs
548
Pathophysiology of radiculopathy?
The point at which spinal nerve roots leave the vertebral column can become narrowed and pinch on the nerve Causing muscle weakness, pain and sensory disturbance
549
Types of radiculopathy?
Cervical radiculopathy Lumbar radiculopathy (sciatica) Thoracic radiculopathy
550
Risk factors for radiculopathy?
Heavy manual labour Poor posture Smoking Operating vibrating equipment Spinal trauma Previous spinal nerve injury
551
Clinical presentation of radiculopathy?
Cervical radiculopathy Numbness and tingling in the fingers, hands Weakness in muscles of the arm, shoulder or hand Loss of sensation in the arms and shoulders Thoracic radiculopathy Sharp, burning, shooting pain present at back, scapula, chest or abdominal wall Lumbar radiculopathy Burning sharp pain radiating down leg
551
Investigations to diagnose radiculopathy?
History and examination; abnormalities in sensation, reflexes, muscle power X-ray; bone alignment MRI/ CT; nerve root compression
552
Differentials for radiculopathy?
Brachial plexus injury Cervical disk injuries Cervical facet syndrome Rotator cuff injury
553
Management for radiculopathy?
Non surgical; rest, physical therapy, NSAIDs, steroid injections Surgical; spinal decompression. discectomy, laminectomy, spinal fusion, foraminotomy, disc replacement surgery
554
Monitoring requirements in radiculopathy?
Annual review with surgeons Monitor for pain, loss of function
555
Complications of radiculopathy?
Prolonged nerve damage Decreased quality of life Cauda equina syndrome Chronic pain syndrome Muscle atrophy, deconditioning and wasting
556
What is cerebellar disease?
Dysfunction of cerebellum resulting in ataxia, coordination, balance and gait disturbance
557
Aetiology of cerebellar disease?
Multiple sclerosis Posterior circulation stroke Bilateral cerebellopontine angle lesions Paraneoplastic syndromes Drugs and toxins Metabolic; thyroid, B12 deficient, coeliac, wilson's disease Infectious; HIV, neurosyphilis, toxoplasmosis GBS Hereditary; friedreich ataxia, Von hippel- lindau syndrome
558
Pathophysiology of cerebellar disease?
Dysregulation of cerebellar activity affects patients gait, balance and coordination
559
Risk factors for cerebellar disease?
Toxin ingestion Poor nutrition Traumatic injury Pre-existing neurological condition
560
Clinical presentation of cerebellar disease?
Nystagmus Hypometric/ hypermetric saccadic eye movements Cerebellar staccato speech Upper limb signs; Intention tremor, Past- pointing, Dysmetria, Dysdiadochokinesis , Hypotonia Truncal ataxia Ataxic gait Heel to shin ataxia
561
Investigations to diagnose cerebellar disease?
Neuroimaging Blood tests; FBC, ESR, CRP, B12, TFT, copper, paraneoplastic screen, auto anti-bodies, tox screen Lumbar puncture
562
Differentials for cerebellar disease?
Parkinson's Dementia Stroke Motor neuron disease Diabetes mellitus Encephalopathy B12 deficiency
563
Management for cerebellar disease?
If cause is identified, treat the cause Physiotherapy and coordination training
564
Monitoring requirements for cerebellar disease?
Regular follow- up with neurologist Serial neuroimaging
565
Complications of cerebellar disease?
Falls Paralysis Dizziness Gait disorder Worsening tremor Psychosocial stigma Raised ICP Developmental delay in children
566
Prognosis of cerebellar disease?
Depends on aetiology Metabolic and nutritional have better prognosis
567
What is the nature of benign brain tumours?
Low grade, less likely to return after treatment
568
What is the nature of malignant tumours?
High grade, more likely to return after treatment
569
Epidemiology of brain tumours?
More prevalent in men and in developed countries Highest incidence in people aged 85 to 89 years
570
Aetiology of brain tumours?
Primary brain tumours originate in the brain Secondary brain tumours have a primary tumour elsewhere and metastasise to brain
571
Pathophysiology of brain tumours?
Creates a space occupying lesion which compresses local structures causing neurological dysfunction If malignant then also has systemic effects of lethargy, weakness, weight loss, fevers
572
Risk factors for brain tumours?
Increasing age Radiation exposure Family history of certain genetic conditions; Tuberous sclerosis, NF1, NF2, turner’s syndrome
573
Clinical presentation of brain tumours?
Headache Seizures Persistent nausea, vomiting, drowsiness Mental, behavioural changes Vision and speech problems
574
Investigations to diagnose brain tumours?
Neuroimaging Bloods
574
Differentials for brain tumours?
Essential tremor Stroke Chronic subdural hematoma Meningitis Orbital optic neuritis AV malformation Intraocular optic neuritis Brain abscess Neurosyphilis
574
Management of brain tumours?
Steroids Pain relief, antiemetics for symptom control Surgery, radiotherapy, chemotherapy
575
Monitoring requirements for brain tumours?
Seek specialist advice Different for different tumours
576
Complications of brain tumours?
Treatment induced toxicity Compression of brain structures Altered mental status Raised ICP
577
Prognosis of brain tumours
Depends on stage and grade of tumour, location and radiological findings
578
Mechanism of action of lamotrigine?
Sodium channel blocker
579
Side effects of lamotrigine?
Stevens- Johnson syndrome
580
Mechanism of action of pyridostigmine?
Acetylcholine esterase inhibitor
581
Side effects of pyridostigmine?
Diarrhoea Vomiting Sweating Muscle cramps/ muscle weakness Increased salivation Miosis Bradycardia Headache

Phase 3A (7 decks)

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