Neurology COPY COPY Flashcards

1
Q

What is a cerebrovascular accident?

A

Ischaemia or infarction of brain tissue secondary to inadequate blood supply
OR
Intracranial haemorrhage

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2
Q

What are the different types of cerebrovascular accidents?

A

Transient Ischaemic Attack(TIA)
Stroke:
Haemorrhagic
Ischaemic

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3
Q

What is a TIA?

A

Sudden onset focal neurological deficit with complete clinical recovery secondary to ischaemia without infarction.

Sx Last <24 hrs

Caused by Reduced blood flow, ischaemia, embolism or disease of blood vessels or blood.

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4
Q

What is a crescendo TIA?

A

where there are two or more TIAs within a week. This carries a high risk of developing in to a stroke.

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5
Q

What is the epidemiology of a TIA?

A

15% of first strokes are preceded by TIA
M > F
Black ethnicity is at greater risk due to their hypertension and atherosclerosis predisposition
20, 000 people have a TIA

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6
Q

What are the risk factors for a TIA?

A

Increasing age
Hypertension
Smoking
Diabetes
Hypercholesterolaemia
Atrial fibrillation
HTN
VSD
Carotid stenosis

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7
Q

What are the causes of a TIA?

A

Thrombus formation or embolus (for example in patients with atrial fibrillation)

Atherosclerosis + embolism from carotid

Shock

Vasculitis

Hyper viscosity - polycythaemia, sickle cell, myeloma

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8
Q

What artery is commonly the route of a TIA?

A

90% = ICA

10% = Vertebral

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9
Q

What are the Clinical features of a TIA?

A

Depends on the site of the TIA:

  • Sudden Loss of function with complete recovery
  • Stroke Sx - Slurred Speech Facial Droop
  • 90% of TIAs affect anterior circulation (ICA)
  • 10% affect Posterior Circulation (vertebral Arteries)
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10
Q

What would be the signs of a TIA in the Anterior Cerebral artery?

A

Weak/numb contralateral leg

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11
Q

What would be the signs of a TIA in the Middle Cerebral Artery?

A

weak/Numb contralateral side of body
Face drooping w/ forehead spared

Dysphasia

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12
Q

What would be the signs of a TIA in the Posterior Cerebral Artery?

A

Vision loss:
Contralateral homonymous hemianopia w/ macula sparing = occipital cortex affected.

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13
Q

What would be the signs of a TIA in the Vertebral Artery?

A

Cerebellar Syndrome: DANISH w/ +tve romberg test

Dysdiadokinesia
Ataxia
Nystagmus
Intention tremor
Slurred staccato speech
Hypotonia

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14
Q

What is Amaurosis Fugax?

A

a painless temporary loss of vision, usually in one eye

Due to occlusion/reduced blood flow to the retina through the ophthalmic, retinal or ciliary artery. (often due to emboli)

This is a bad sign as it often signals stroke is impending

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15
Q

What is the Primary investigation for a TIA?

A

Diagnosis is Clinically made: Usually TIA/Stroke is obvious
ABCD^2 assessment
FAST test

MRI - First line for confirmation
Carotid Doppler - Look for Stenosis
CT angiography - Look for Stenosis
ECG

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16
Q

What is the FAST acronym?

A

FACE
ARMS
SPEECH
TIME

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17
Q

What is the ABCD^2 scoring system for TIA/Stroke?

A

No longer recommended by NICE

Age >60
BP >140/90
Clinical Sx - Unilateral Weakness (+2). Speech Disturbance w/o weakness (+1)
Duration >1hr (+2) / <1hr (+1)
DM - Type 2

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18
Q

What would be a high or low risk score following ACBD^2 assessment for TIA/stroke?

A

High risk:
ABCD2 score of 4 or more
AF
More than TIA in one week
TIA whilst on anti-coagulation

Low risk:
None of the above
Present more than a week after their last symptoms have resolved

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19
Q

How can you distinguish between a TIA and a Stroke?

A

You cant until after recovery

TIA Sx resolve usually within/<24 hours

Stroke Sx last more than 24 hours

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20
Q

What is the management of a High and low Risk TIA?

A

Lower RFs - stop smoking, reduce alcohol, exercise and diet

Immediate Aspirin 300mg

Start secondary prevention of CVD:
Clopidogrel 75mg
Atorvastatin 80mg
Treat BP - Ramipril

High Risk - Refer for specialist assessment within 24 hours of onset of symptoms
Low Risk - Refer for specialist assessment within 7 days of onset of symptoms

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21
Q

What are the main complications of a TIA?

A

Increased risk of stroke
Increased risk of underlying CVD

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22
Q

What are the two types of stroke?

A

Ischaemic (85% of cases)
Haemorrhagic (15% of cases)

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23
Q

Define a stroke?

A

Rapid onset neurological deficits caused by focal, cerebral, spinal or retinal infarction lasting more than 24 hrs

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24
Q

What is the epidemiology of a stroke?

A

1.2 million people living with stroke in the UK

110, 000 people have a first or recurrent stroke per year

Uncommon in those under 40

More common in males than females

Incidence is falling due to more vigorous approach to risk factors in primary care e.g. statin use and BP control

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25
What is an Ischaemic Stroke?
85% of strokes An episode of neurological dysfunction caused by focal cerebral, spinal or retinal infarction secondary to the occlusion of a blood vessel
26
What are the categories of Ischaemic Stroke?
Large Vessel Disease (50%) - Atherosclerosis Small Vessel Disease (25%) - Lacunar Cardioembolic (20%) - AF, IE, MI, Dissection Cryptogenic (<5%) Rare causes (<5%) - vasculitis
27
What are the main causes of Ischaemic stroke?
Large artery stenosis Cardiac emboli from AF, MI or infective endocarditis 🡪 blood stasis Atherothromboembolism e.g. from carotid artery Dissection of aorta/carotid Shock – reduced blow flow throughout body Vasculitis
28
What is a Haemorrhagic Stroke?
15% of strokes: Rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system not caused by trauma.
29
What are the subtypes of haemorrhagic stroke?
Primary Intracerebral: bleeding within the brain parenchyma Subarachnoid Haemorrhage: bleeding into the subarachnoid space Secondary haemorrhage (these are NOT strokes) - due to trauma, anti-coagulation (warfarin), Bleeding due to tumour
30
What are the main causes of a haemorrhagic stroke?
Hypertension Aneurysm rupture 🡪 SAH Arteriovenous Malformation (AVM) Amyloidosis
31
What is the 3rd leading cause of mortality in the US and UK?
Stroke
32
What are the risk factors for stroke?
Hypertension - greatest RF Increased age - 68-75 MC Male Smoking Diabetes Hypercholesterolaemia AF Heart disease FHx Medication
33
What are the symptoms of stroke?
Focal neurological deficit based on site of the infarct.
34
What would be an extra finding in haemorrhagic stroke?
Increased intracranial pressure (ICP) Causes midline shift
35
What is a Lacunar Stroke?
Very common type of ischaemic stroke of the lenticulostriate arteries. These supply the deep brain structures (BG, IC, Thalamus, pons)
36
What are the clinical manifestations of a stroke in the anterior cerebral artery?
Contralateral weakness of lower limb Contralateral sensory loss of lower limb Truncal ataxia Incontinence Drowsiness Dysphasia (if dominant hemisphere) Logical thinking Personality
37
What are the clinical manifestations of a stroke in the Middle cerebral artery?
Contralateral motor weakness – arms and legs Hemiplegia – paralysis of one side of the body Contralateral sensory loss Aphasia – inability to understand (Wernicke’s) or produce speech (Broca’s) Dysphasia (speech problems) – only if stroke is in dominant hemisphere (Broca’s) Facial droop
38
What are the clinical manifestations of a stroke in the Posterior cerebral artery?
Contralateral homonymous hemianopia with macular sparing Visual agnosia Disorders of Perception
39
What are the clinical manifestations of a stroke in the Vertebrobasilar artery?
Cerebellar signs Reduced consciousness Disorders of balance Coordination disorders Quadriplegia or hemiplegia
40
What are the clinical manifestations of a stroke in Weber’s syndrome (midbrain infarct; branches of posterior cerebral artery)
Oculomotor palsy and contralateral hemiplegia
41
What are the clinical manifestations of a stroke in Lateral medullary syndrome (posterior inferior cerebellar artery occlusion)
Ipsilateral facial loss of pain and temperature Ipsilateral Horner’s syndrome Ipsilateral cerebellar signs Contralateral loss of pain and temperature
42
What is horner's Syndrome?
Caused by a Lesion within the Sympathetic Pathway Presents as a unilateral triad of: Miosis: small pupil Ptosis: drooping eyelid Anhidrosis: lack of sweat
43
What are the clinical manifestations of a stroke in the Basilar Artery?
Locked in syndrome; Paralysed except for muscles that control eye movements. Px are consciously aware, can think and reason but cannot speak or move
44
What are the extra symptoms of a haemorragic stroke?
headache AMS (altered Mental Status) Seizures N+V
45
What are the primary investigations for a stroke?
CT Head: Ischaemic - mostly normal Haemorrhagic - Hyperdense blood Ix over first few days after stroke: MRI - with diffusion weighted imaging CT Angiography Carotid Doppler USS ECHO - for those with cardioembolic stroke ECG - For AF Bloods - rule out hypoglycaemia
46
What is the very first step in the acute management of a suspected stroke?
Determine if the stroke is haemorrhagic or ischaemic from the initial CT.
47
What is the management for an Ischaemic stroke?
immediate CT to exclude primary intracerebral haemorrhage If presents within 4.5hrs: Clot buster (thrombolysis) - IV Alteplase Presenting After 4.5 hrs Aspirin 300mg for 2 weeks Prophylaxis - Lifelong clopidogrel (75mg)
48
What is the function of Alteplase? What are the contraindications?
Tissue plasminogen activator that rapidly breaks down clots and can reverse the effects of a stroke if given in time. CIs: Haemorrhage, Intracranial bleed, clotting disorders, aneurysms
49
What is the management of a Haemorrhagic Stroke?
Neurosurgery referral for larger bleeds Control BP - BB/ARB to <150 systolic Iv mannitol for increased ICP Vitamin K if bleeding is warfarin related rehabilitation - Physio/OT
50
What type of stroke should be suspected if the patient is on oral anticoagulants?
Suspect Haemorrhagic until proven otherwise
51
What are some key differential diagnoses for strokes?
Hypoglycaemia Space occupying Lesions - tumour, AVM Syncope due to arrythmia Migraines Functional Neurological Disorders Infection - particularly in elderly
52
What is the prophylactic prevention of secondary strokes?
Clopidogrel 75mg once daily (alternatively dipyridamole 200mg twice daily) Atorvastatin 80mg should be started but not immediately Carotid endarterectomy or stenting in patients with carotid artery disease Treat modifiable risk factors such as hypertension and diabetes
53
What is a haematoma?
Describes a bleed that has mostly clotted and hardened
54
What is a Haemorrhage?
Describes an active ongoing bleed
55
Where can intracranial haemorrhages occur?
Extradural Subdural Subarachnoid Intracerebral
56
What are the main blood vessels within the meninges?
Extradural – middle meningeal artery Subdural – bridging veins Subarachnoid – circle of Willis Pia – no vessels as it forms part of the blood-brain barrier
57
What is an Extradural (Epidural) haemorrhage (EHD)?
Bleeding into the potential space between the skull and the dura mater. The blood then collects in this space and is referred to as an extradural haematoma (EDH).
58
What are the causes of Extradural haemorrhage?
Usually Trauma (blunt trauma): Arterial bleed - often middle meningeal artery Venous bleed - often due to dural venous sinus
59
What is the most common blood vessel damaged to cause an extradural bleed?
Middle meningeal artery due to damage to the pterygoid bone
60
What are some rarer causes of an EDH?
Non-traumatic: Haemorrhagic tumour Coagulopathy Infection Vascular Malformation
61
What are the risk factors for an EDH?
Younger age (20-30) Male Anticoagulant usage
62
Why is an EDH less likely to occur in the elderly?
The Dura matter is more firmly adhered to the skull so blood is less likely to accumulate in this region.
63
What is the typical presentation of an Extradural bleed?
Characteristic history: Head injury Loss of consciousness following trauma or initial drowsiness Lucid interval – period of time between traumatic brain injury and decrease in consciousness Signs of raised ICP – headache, vomiting, nausea, seizure ± hemiparesis with brisk reflexes Cushing's Triad - Bradycardia and raised BP and Respiratory Irregularity Ispilateral pupil dilation Decreased Glasgow coma scale Coning of brain through foramen magnum Death due to respiratory arrest
64
What are the cushings triad signs of an extradural haemorrhage?
Wide Pulse Pressure Bradycardia Respiratory irregularity
65
Why is there an increased ICP in an EDH?
Haemorrhage - increased volume decreased pressure old blood clots which can then take up water (osmotically active) Will increase in volume and raise ICP
66
What are the primary investigations of an EDH?
CT head: Lens shaped hyperdense bleed/haematoma Confined within suture lines Midline shift Skull XR - may show fracture
67
What is the management on an EDH?
Urgent Neurosurgery referral: - Burr Hole craniotomy Ligation of bleeding vessel Stabilise Px - ABCDE management IV Mannitol to reduce ICP
68
What are the complications of an EDH?
Cerebral oedema Raised intracranial pressure and herniation Ischameia: can occur due to mass effect, herniation, hypoperfusion, vasospasm Seizures Infection
69
What is the Typical History of an EDH?
The typical history is a young patient with a traumatic head injury that has an ongoing headache. They have a period of improved neurological symptoms and consciousness followed by a rapid decline over hours as the haematoma gets large enough to compress the intracranial contents.
70
What are some Key differential Diagnoses of an EDH?
Subdural haematoma Subarachnoid haematoma Epilepsy Meningitis Carotid dissection Carbon monoxide poisoning – fit with lucid period
71
What is a Subdural Haemorrhage?
When blood accumulates in between the dura and arachnoid matter often due to rupture of the bridging veins
72
What are the causes of a Subdural haemorrhage?
Often due to the rupture of a bridging vein caused by trauma: Shearing deceleration injury Abused children (shaken baby sydrome)
73
What is the Epidemiology of a Subdural Haemorrhage?
Often in Px who have small brains: Alcoholics, Dementia, Children Occurs in Abused Children (Shaken Baby Syndrome)
74
What are the risk factors for a subdural haemorrhage?
Increased age alcoholics Trauma Cortical atrophy (due to age/dementia) Child abuse
75
What is the pathology of a SDH?
- Trauma either due to deceleration due to violent injury or due to dural metastases results in bleeding from bridging veins between cortex and venous sinuses - Bridging veins bleed and form a haematoma (solid swelling of clotted blood) between the dura and arachnoid - This reduces pressure 🡪 bleeding stops - Days/weeks later the haematoma starts to autolyse due to the massive increase in oncotic and osmotic pressure 🡪 water is sucked into the haematoma 🡪 haematoma enlargement 🡪 gradual rise in intra-cranial pressure (ICP) over many weeks - This shifts midline structures away from the side of the clot and can lead to tectorial herniation and coning (brain herniates through foramen magnum) if left untreated
76
What are the symptoms of a subdural haemorrhage?
Often gradual symptom onset with a latent period (can be days, weeks, months) Progressive confusion and cognitive deficit Headaches and vomiting Focal neurological deficit, e.g. weakness or fixed dilated pupil Fluctuating consciousness
77
What are the clinical signs of a subdural haemorrhage?
Signs of Raised ICP - headache, N+V, Seizure Cushing Triad - Wide PP, Bradycardia, Resp irregularity Fluctuating GSC Herniation - Supratentorial and infratentorial
78
What are the primary investigations of a subdural haemorrhage?
CT Head: Banana/Crescent shaped dense region. Not confined to suture lines. May have midline shift If acute - Hyperdense (bright) If Subacute - Isodense If Chronic - Hypodense (darker than brain
79
What is the treatment for a subdural haemorrhage?
Referral To Neurosurgeon IV mannitol - reduce ICP Burr hole / Craniotomy to relieve pressure
80
What is a subarachnoid haemorrhage (SAH)?
Subarachnoid haemorrhage involves bleeding in to the subarachnoid space, where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane. This is usually the result of a ruptured cerebral aneurysm.
81
What is the Epidemiology of a Sub Arachnoid Haemorrhage?
Typical age 35-65 – mean age 50 Account for ~5% of strokes 8-12 per 100, 000/year
82
What are the possible causes of an SAH?
Trauma Non-Trauma: (spontaneous) Berry Aneurysm from circle of willis- MC of spontaneous SAH (70%) AVM
83
Where do berry aneurysms often occur?
Usually at junctions of arteries within the circle of Willis. Often communicating junctions
84
What is the most common artery affected in an SAH?
Circle of Willis: Anterior communicating artery ACA junction
85
What are the risk factors for a SAH? What are some strong associations with SAH?
Increased age - >50yrs HTN Known Aneurysm PKD Trauma FHx Smoking Alcohol excess Strong associations with Cocaine Use and Sickle Cell
86
What is the Pathology of an SAH from a Berry Aneurysm?
Rupture of the arteries forming the circle of Willis Rupture of the junction of the anterior communicating artery and the anterior cerebral artery or the posterior communicating artery and the internal carotid artery Leads to tissue ischaemia (since less blood can reach the tissue) as well as rapid raised ICP as the blood acts like a space-occupying lesion and puts pressure on the brain 🡪 neurological deficits
87
What is the Pathology of an SAH from an AVM?
Atriovenous malformations (AVM) Vascular development malformation often with a fistula between arterial and venous systems causing high flow through the AVM and high-pressure arterialisation of draining veins 🡪 rupture
88
What are the symptoms of a SAH?
Occipital Thunderclap Headache Seizures Vomiting Loss of Consciousness - Coma/Drowsiness Meningism (mimics meningitis) Reduced GSC Nerve palsies - 3rd / 6th
89
What are the signs of an SAH?
Meningeal irritation: - Kernig’s sign – unable to extend patient’s leg at the knee when the thigh is flexed - Neck stiffness - Brudzinski’s sign – when patient’s neck is flexed, patient will flex their hips and knees Subhyaloid haemorrhages (bleeding between retina and vitreous membrane) ± papilloedema
90
What are the characteristics of the headache experienced in an SAH?
Occipital Thunderclap Headache Sudden onset Worst headache of their life (0-10 instantly) May have a sentinel headache preceding this
91
Why may you get nerve palsies in SAH?
3rd nerve palsy: An aneurysm arising from the posterior communicating artery will press on the 3rd nerve, causing a palsy with a fixed dilated pupil 6th nerve palsy: A non-specific sign which indicates raised intracranial pressure
92
What are the primary investigations in a SAH?
CT Head - diagnostic with 100% sensitivity if performed within 6 hrs. If Negative but SAH still suspected: Lumbar Puncture (performed after 12hrs) will show xanthochromia / yellowish CSF due to RBC haemolysis Angiography (CT or MRI) can be used once a subarachnoid haemorrhage is confirmed to locate the source of the bleeding. ABG - Rule out hypoxia
93
Who do SAHs more commonly affect?
Black patients Female patients Age 45-70
94
What is the Glasgow Coma Scale (GCS)?
Tool for assessing consciousness: Based on Eyes, verbal and motor response. Normal - 15/15 Comatose - 8/15 Unresponsive - 3/15 Eyes: Spontaneous = 4 Speech = 3 Pain = 2 None = 1 Verbal response: Orientated = 5 Confused conversation = 4 Inappropriate words = 3 Incomprehensible sounds = 2 None = 1 Motor response: Obeys commands = 6 Localises pain = 5 Normal flexion = 4 Abnormal flexion = 3 Extends = 2 None = 1
95
What are important differential diagnoses of SAH?
Meningitis - no thunderclap headache in this Migraine - no meningism/thundercap headache in this
96
What is the treatment for an SAH?
1st line: Neurosurgery Referral: 1st - Endovascular coiling 2nd - Surgical clipping Give immediate Nimodipine (CCB) 60mg (every 4 hrs for 21 days)- prevents vasospasm Resuscitation Monitoring for complications
97
What are some complications of an SAH?
Re-bleeding Cerebral ischaemia - due to vasospasm Hydrocephalus – due to blockage of arachnoid granulations Hyponatraemia - due to urinary salt loss
98
What are some Differential Diagnoses of an SAH?
Migraine Meningitis Corticle vein thrombosis
99
What is an Intracerebral haemorrhage?
Intracerebral haemorrhage involves bleeding into the brain tissue. It presents similarly to an ischaemic stroke. Often has a headache/come and signs of raised ICP
100
Define Meningitis?
Inflammation of the meninges This is a notifiable condition to PHE
101
What are the different causes of Meningitis?
Viral: Enterovirus (coxsackie) HSV2 VZV Bacterial: N. Meningitidis S. pneumonia
102
What is the most common cause of meningitis?
Viral cause
103
What organism is the most common cause of viral and bacterial meningitis?
Viral - Enterovirus (coxsackie) Bacterial - S. pneumoniae
104
Which is a more severe form of meningitis?
Bacterial is more severe
105
What is the pathology of Meningitis?
- Brain and the CSF should be sterile – no bacteria - Bacteria can get in through different routes: - Neurosurgical complications: post-op, infected shunts, trauma - Extracranial infection: ear – otitis media, nasopharynx, sinuses – sinusitis - Via the blood stream: i.e. bacteraemic seeding - Once the CSF is infected the pathogen can multiply and replicate because there are no immune cells (as the BBB prevents the movement from the blood) - Eventually the WBCs enter into the CSF, meninges and brain due to the blood vessels becoming leaky - This causes meningeal inflammation +/- brain swelling
106
What are the main risk factors for meningitis?
Extremes of age (Infant/elderly) Immunocompromised Pregnancy Travel Crowded environment - barracks/uni Non-vaccinated
107
What is the most common bacterial cause of meningitis in neonates (0-3 months)?
Group B Strep (S. agalactiae) Due to the colonisation of mothers vagina which can cause infection in neonate at birth. Also E.coli and Listeria
108
What is the most common bacterial cause of Meningitis in Infants?
N. meningitidis S. pneumoniae H. Influenzae (now rare due to vaccine)
109
Why is Haemophilus influenzae now a less common cause of meningitis?
Due to vaccination
110
What are the common bacterial causes of meningitis in adults?
S. pneumoniae N. Meningitidis
111
What are the most common bacterial causes of meningitis in the elderly?
S. pneumoniae N. meningitidis Listeria
112
What are the most common bacterial causes of meningitis in the immunocompromised?
Listeria monocytogenes M. Tuberculosis
113
What vaccines are available for meningitis coverage?
N. Meningitidis - Men B + Men C + Men ACWY S. pneumoniae - PCV Vaccine
114
What is meningococcal Septicaemia?
N. meningitidis infection in the blood. This causes a non-blanching purpuric rash This is due to Disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhages
115
What are the symptoms of Meningitis?
Meningism: Headache, Photophobia, Neck stiffness Fever Nausea + Vomiting Seizures Purpuric Rash - Bacterial Meningitis Non-Blanching Purulent Rash - Meningococcal Septicaemia
116
What are the clinical signs of meningitis?
Kernig's Sign: When the hip is flexed and the knee is at 90°, extension of the knee results in pain Brudzinski Sign: severe neck stiffness causes the hips and knees to flex when the neck is flexed
117
What are the primary investigations in meningitis?
Bloods: FBC - raised WCC CRP - raised Blood glucose - compared with CSF Blood culture - to determine viral/bacterial CT Head - Look for Brain Lesions/Abscesses/CIs for LP GS DIAGNOSTIC = Lumbar Puncture (LP) + CSF Analysis
118
What are some contraindications for a lumbar puncture?
Raised ICP GCS <9 Focal Neurological signs
119
Where is a lumbar puncture usually taken from?
Between L3/L4 Since spinal cord ends L1/2
120
What would the results of an LP CSF sample analysis look like in bacterial meningitis?
CSF: Appearance - Cloudy WCC - High neutrophils Protein High Glucose - Low Culture - bacterial organism bacteria swimming in the CSF (cloudy) will release proteins (high) and use up the glucose (low). Immune response to bacteria is neutrophils
121
What would the results of an LP CSF sample analysis look like in Viral meningitis?
CSF: Appearance - Clear WCC - High Lymphocytes Protein - Normal/Mildly raised Glucose - Normal Culture - Negative Viruses cant be seen (clear) don’t use glucose (normal) but may release a small amount of protein (normal/mild inc). Immune response to viruses are lymphocytes
122
What is the treatment for viral Meningitis?
Usually milder and so Supportive Tx If HSV/VZV infection then Acyclovir
123
What is the treatment for bacterial meningitis in a hospital?
Broad Spec Abx - Cover All Likely Organisms: 1st Line - Ceftriaxone or Cefotaxime (as they get through the BBB) WTIH OR AFTER IV Dexamethasone - Prevent neurological sequelae 2nd Line: Chloramphenicol Once Blood cultures have been done then can tailor Abx: Eg. IV Benzylpenicillin for N.Meningitidis
124
What is the treatment for suspected meningitis w/ non-blanching rash present in the community?
Suspected Meningococcal infection: Urgent/immediate IM Benzylpenicillin Prior to immediate transfer to a hospital (unless it will cause a delay)
125
What are some complications of meningitis?
Hearing loss is a key complication Seizures and epilepsy Cognitive impairment and learning disability Memory loss Cerebral palsy, with focal neurological deficits such as limb weakness or spasticity
126
What are some Differential Diagnoses of Meningitis?
‘Worst headache ever’ - subarachnoid haemorrhage (especially if trauma, ‘thunderclap onset’) migraine Encephalitis flu and other viral illnesses sinusitis brain abscess malaria
127
What are some specific complications related to meningococcal meningitis?
Risk of DIC Risk of Waterhouse Friedrichsen Syndrome
128
What is Waterhouse Friedrichsen Syndrome?
Adrenal insufficiency caused by intra-adrenal haemorrhage as a result of meningococcal DIC
129
What is the most common cause of fungal meningitis?
Cryptococcus Neoformans Candida Only really affects immunocompromised Px
130
What can be given to close contacts of a Px who has Meningitis?
Rifampicin Ciprofloxacin
131
What is Encephalitis?
infection of the brain leading to inflammation of the brain parenchyma
132
What are the causes of Encephalitis?
Viral (most common) Also bacterial, fungal, parasitic, paraneoplastic
133
What is the most common cause of encephalitis?
HSV-1 Accounts for 95% of the cases Also CMV, EBV, HIV, VZV
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What are the risk factors of encephalitis?
Immunocompromised Extremes of age Transfusion/Transplantation
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Why can close contact with cats be a risk factor for encephalitis?
Risk of toxoplasmosis infection
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What are the symptoms of encephalitis?
Px often has preceding flu like Sx Triad Of: Fever Headache Altered GCS: Behavioural changes/Psychotic behaviour/mood changes Confusion Focal Neurological deficit Memory loss Seizures
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What are the clinical signs of encephalitis?
Pyrexia Reduced GCS Focal neurological deficit: Aphasia Hemiparesis Cerebellar signs
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What is the most common place to be affected by encephalitis?
Temporal and inferior frontal lobe
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What are the primary investigations for encephalitis?
Bloods - FBC, CRP, U&Es MRI head – to show swelling/ inflammation ± midline shifting due to raised ICP EEG – shows periodic sharp and slow waves Lumbar puncture (after): raised lymphocytic CSF, viral PCR HIV TEST – acute phase viraemia can cause encephalitis
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What is the treatment of encephalitis?
Mostly Supportive IV Acyclovir - for HSV/VZV
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What is multiple sclerosis?
Chronic progressive autoimmune, T-cell mediated inflammatory disorder of the CNS against the myelin basic protein of oligodendrocytes causing demyelination of CNS neurons. It occurs sporadically over years
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What type of reaction is MS?
Type 4 Hypersensitivity Reaction: T-Cell mediated
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What is the Epidemiology of MS?
Women to Men – 2:1 Usually diagnosed between 20-40 = disease of the young More common the further from the equator you go (possible a link to Vitamin D) – explains why it is exacerbated by heat
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What are the risk factors for MS?
Females 20-40 Autoimmune disease FHx - Associated with HLA-DR2 EBV exposure in childhood
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What is the pathophysiology of MS?
Type IV Hypersensitivity Rxn: T-cell mediated – T cells activate B cells to produce auto-antibodies against Basic myelin protein of oligodendrocytes T Lymphocytes manage to cross the BBB, they can cause a cascade of destruction to the neuronal cells in the brain by recruiting other immune cells This results in plaques of demyelination and inflammation and therefore conduction disruption along axons Although the myelin sheath does regenerate, the new myelin is less efficient and temperature dependent Therefore Symptoms are exacerbated by heat
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Where do the plaques of Demyelination occur in MS?
Often Perivenular (but can occur anywhere in the CNS) Commonly at: Optic nerves - blurred vision Ventricles of the brain Corpus Callosum Brainstem and cerebellum connections Cervical Spinal Cord
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What are the features of pathological lesions in Active MS?
- Demyelination – breakdown products present - Variable oligodendrocytes - Hypercellular plaque edge due to infiltration of tissue with inflammatory cells - Perivenous inflammatory infiltrate (mainly macrophages and T-lymphocytes) - Extensive BBB disruption - Older active plaques may have central gliosis
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What are the features of pathological lesions in Inactive MS?
- Demyelination – breakdown products absent - Variable oligodendrocytes loss - Hypocellular plaque - Variable inflammatory infiltrate - Moderate to minor BBB disruption - Plaques gliosed
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What are the different Classifications of MS?
- Pattern 1 – macrophage mediated - Pattern 2 – antibody mediated Lots of inflammation, those patients respond to certain therapies such as plasma exchange - Pattern 3 – distal oligodendrogliopathy and apoptosis (ischaemic/toxic, virus induced) - Pattern 4 – primary oligodendroglia degeneration (metabolic defect)
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What are the types of MS Progression?
Relapse - Remitting: The most common pattern (85% of cases) Episodic flare-ups (may last days, weeks or months), separated by periods of remission Secondary Progressive: Starts with relapse remitting Gets progressively worse w/o remission Primary Progressive: Symptoms get progressively worse from disease onset with no periods of remission Progressive/relapsing: Progressive disease from onset, with clear acute relapses, with or without full recovery, with periods between relapses characterised by continuing progression
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What is Uhtohoff's Phenomenon?
worsening of neurological symptoms in MS when body gets overheated from hot weather, exercise, saunas and hot tubs, showers
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What percentage of MS patients progress from relapse remitting to secondary progressive MS?
60-75% progress within 15 years
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What are the causes of MS?
Unclear cause for demyelination but: Multiple genes Epstein–Barr virus (EBV) Low vitamin D Smoking Obesity combination of these have an influence
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What is the presentation of MS?
Variable presentation depending on region affected Sx progress over 24 hrs and can last days-weeks and then Improve
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What are the General symptoms of MS?
Charcot's Triad: - Dysarthria - Plaques in the brainstem - Intention Tremor - Plaques along motor pathways - Nystagmus - Plaques in nerves of eyes - Spinal cord Weakness Paraplegia Spasticity Tingling Numbness - Optic nerves Impaired vision Eye pain Medulla and pons Dysarthria Double vision Vertigo Nystagmus - Cerebellar white matter Dysarthria Nystagmus Intention tremor Ataxia
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What are the clinical signs of MS?
- Typical – LOSS NB L - Lhermitte’s sign - electric shock runs down back and radiates to limbs O - Optic neuritis – impaired vision and eye pain S - Spasticity and other pyramidal signs S - Sensory symptoms and signs N - Nystagmus, double vision and vertigo - 6th nerve palsy B - Bladder and sexual dysfunction - Exacerbated by heat – showers, hot weather, saunas (Uhthoff’s phenomenon) - Improved by cool temperatures
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What are the primary investigations for MS?
Clinical Dx (using McDonald criteria) and Sx progression/remission Contrast MRI of Brain and spinal cord: Used to support Dx by identification of demyelinating plaques LP w/ CSF Electrophoresis - may show oligoclonal IgG bands in CSF Evoked Potentials - Test length of time of impulse travel
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What is the McDonald Criteria?
Criteria used to diagnose MS: - 2 or more CNS lesions disseminated in time and space - Need to be sure it affects two parts of nervous system e.g. brain and spinal cord, optic nerve and brain - More than one attack spaced out in time e.g. optic neuritis last year, now present with weakness in both legs
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What would the results of the McDonald Criteria be to diagnose MS?
2 or more relapses AND EITHER Objective clinical evidence of 2 or more lesions OR Objective clinical evidence of one lesion WITH a reasonable history of a previous relapse (Objective evidence’ is defined as an abnormality on neurological exam, MRI or visual evoked potential)
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Who manages MS?
MDT: including neurologists, specialist nurses, physiotherapy, occupational therapy and others.
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How can acute relapses of MS be treated (Relapse-Remitting MS)?
Steroids: IV Methylprednisolone + Sx treatment of Complications: Depression - SSRIs Neuropathic pain - Gabapentin Exercise - maintain strength
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How can Chronic MS be treated long term?
1st line (frequent relapse): – SC beta interferon and glatiramer acetate 2nd line (disease modifying): - IV alemtuzumab – CD52 monoclonal antibody that targets T cells - IV natalizumab – acts against VLA-4 receptors that allow immune cells to cross the BBB and therefore reduces number of immune cells that can enter the CNS and cause damage
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What are the side effects to Beta Interferon injections used to treat MS?
Injection site reactions Flu-like symptoms Mild intermittent lymphopenia Mild to moderate rises in liver enzymes Most common S/E (e.g. flu-like symptoms) tend to decrease after the first few months of treatment
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What is Guillain Barre Syndrome?
Guillain-Barré syndrome (GBS) is an autoimmune, rapidly progressive demyelinating condition of the peripheral nervous system, often triggered by infection (URTI/GI) "Equivalent to MS for the PNS"
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What is the Epidemiology of Guillain Barre Syndrome?
More common in males Peak ages 15-35 and 50-75 Most common acute polyneuropathy
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What are the causes of Guillain Barre Syndrome?
Usually triggered post infection (6 weeks) and strongly associated with: Campylobacter jejuni (most common) CMV EBV
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What is the most common cause of Guillain Barre Syndrome?
Post C. jejuni infection
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What is the most common type of Guillain Barre Syndrome? What are the 3 classical symptoms of this type?
Acute demyelinating inflammatory polyneuropathy (ADIP) in 90% of cases Presents with: Progressive symmetrical weakness in limbs Reduced or absent tendon reflexes Reduced sensation
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What is the pathophysiology of Guillain Barre Syndrome?
Molecular Mimicry: A pathogenic antigen (e.g. Campylobacter jejuni) resembles myelin gangliosides in the peripheral nervous system The immune system targets the antigen of pathogen and subsequently and attacks the similar antigen of the myelin sheath of sensory and motor nerves Schwann Cells Nerve cell damage consists of damage to the Schwann cells and therefore segmental demyelination 🡪 reduction in peripheral nerve conduction 🡪 an acute polyneuropathy This autoimmune process involves the production of anti-ganglioside antibodies (anti-GMI is positive in 25% of patients) The demyelination causes polyneuropathy
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What are the risk factors for Guillain Barre Syndrome?
History of respiratory or GI infections 1-3 weeks prior to onset Vaccinations have been implicated e.g. flu vaccine Post pregnancy – incidence decreases during pregnancy but increases in months after delivery
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What are the symptoms of Guillain Barre syndrome?
Recent Hx of Infection (GI/URTI) Paraesthesia and numbness Muscle weakness Back and limb pain CN involvement – diplopia and dysarthria Respiratory – affects diaphragm 🡪 death - Autonomic features Sweating Raised pulse Postural hypotension Arrhythmias
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What are the clinical signs of Guillain Barre Syndrome?
Reduced sensation in limbs Ascending Symmetrical weakness - lower extremities first (proximal then distal) Loss of deep tendon reflexes (hyporeflexia) Autonomic dysfunction - Tachycardia, HTN, postural hypotension etc. Respiratory distress - RF in 35% of patients
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What are the primary investigations for Guillain Barre syndrome?
Lumbar Puncture (L4) - Raised protein + normal WCC = inflammation but no infection Nerve conduction studies: Conduction velocity reduced/blocked Lung Function Tests (spirometry) - Decreased FVC
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What investigations can aid to confirm the diagnosis of Guillain Barre?
Ix to exclude other causes: TFTs - Hypothyroidism for cause of weakness U&Es - Electrolytes for neuropathic issues Spirometry - measure lung function
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What is the management of Guillain Barre syndrone?
First line: IV Ig (immunoglobulin) for 5 days - reduces duration and severity of paralysis + Plasmapheresis - to remove autoantibodies LMWH (enoxaparin) reduce risk of venous thrombosis
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What is the prognosis of Guillain Barre?
Good prognosis 85% make a full recovery
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When may Ig treatment for Guillain Barre be contraindicated?
If patient is IgE deficient May cause an allergic reaction
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What are some Differential Diagnoses of Guillain Barre Syndrome?
Other causes of NM paralysis Hypokalaemia Polymyositis Myasthenia gravis Botulism Poliomyelitis
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What is Huntington's Chorea (HD)?
A Neurodegenerative Autosomal dominant genetic condition causing chorea characterised by the lack of the main inhibitory neurotransmitter GABA
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What is the penetrance of HD?
Full penetrance: All genotypes of Huntington's will express the phenotype Also shows Anticipation
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What are the genetics related to HD?
Huntington’s chorea is a “trinucleotide repeat disorder” that involves a genetic mutation in the Huntingtin (HTT) gene on chromosome 4. Need >36 Triplet CAG repeats affecting HTT gene to be diagnostic of HD
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What is a common feature of tri-nucleotide repeat disorders in terms of prevalence?
They Show anticipation: where successive generations have more repeats in the gene, resulting in: Earlier age of onset Increased severity of disease
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What is the Pathology of Huntington's Chorea?
Repeated CAG sequence leads to translation of an expanded polyglutamine repeat sequence in the huntingtin gene The more CAG repeats present, the earlier symptoms present Faulty Huntingtin protein builds up in the striatum causing cell death and loss of cholinergic and GABA-nergic neurons 🡪 decreased ACH and GABA synthesis in striatum Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels resulting in excessive thalamic stimulation and subsequently increased movement (chorea)
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When do symptoms of HD usually present?
Often ASx in patients under 30 yrs Sx present between 30-50 yrs initially with a prodromal phase of mild Sx People with HD will have more severe symptoms typically around 60+ yrs
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What are the symptoms of HD?
Insidious progressive worsening: Starts with cognitive, psychiatric and mood problems (around middle age) Then can progress to: Chorea (involuntary, abnormal movements) Eye movement disorders dysarthria dysphagia
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How is a Diagnosis of HD made?
Clinical diagnosis with FHx HD and subsequent generations showing anticipation. Genetic testing - >36 CAG repeats on chromosome 4 MRI/CT - Shows atrophy of striatum
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What is the treatment of HD?
No Tx to stop or progress HD Provide Extensive counselling and support Can provide Sx treatment for chorea: Chorea: Antipsychotics (olanzapine) - Dopamine Receptor antagonists Benzodiazepines (diazepam) Dopamine-depleting agents (tetrabenazine) Depression - SSRI (sertraline)
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What is the prognosis of HD?
Progressive uncurable condition Life expectancy of 15-20 years post diagnosis Death in HD most commonly caused by aspiration pneumonia or Suicide
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What are some differential diagnoses for chorea such as in HD?
HD Sydenham’s chorea (rheumatic fever) SLE Basal ganglia stroke Wilson’s disease
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What are the causes of depression?
Psychiatric: Anxiety Alcohol abuse Substance misuse Grief Physical: Parkinson’s MS Endocrine Medication – Beta-blockers, combined OCP CV accident (stroke) Learning difficulties
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What are the symptoms of Depression?
Low mood – loss of interest in activities they used to enjoy Appetite and weight change Sleep pattern changes – sleeping too much/difficult sleeping Fatigue Lack of concentration or making decisions Feelings of worthlessness or excessive/inappropriate guilt Self-harm and suicide
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How can Depression be treated/managed?
Mental health team – crisis team - IAPT CBT Counselling Medication Selective Serotonin Reuptake Inhibitors e.g. fluoxetine, sertraline Prevent the presynaptic neuron from reabsorbing serotonin so more remains in synaptic cleft and can stimulate receptors on post synaptic neuron (in pre-frontal cortex) Tricyclic antidepressants e.g. amitriptyline and amoxapine Act on muscarinic receptors Information/education
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What is Parkinson's Disease (PD)?
A progressive neurodegenerative movement disorder characterised by loss of dopaminergic neurones within the substantia nigra pars compacta (SNPC) of the basal ganglia (nigrostriatal pathway).
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What is the Epidemiology of PD?
The second most common neurodegenerative disorder after dementia Prevalence increases with age (peak onset 55-65) More common in males
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What are the risk factors for PD?
Increased age Male FHx
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What is the peak age of onset for PD?
55-65 yrs
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What are the causes of PD?
Idiopathic condition but potentially related to genetics There are secondary causes of parkinsonism: Drugs/Toxins - CO Wilsons disease Infections - Encephalitis, Creutzfeldt-Jakob Disease
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What are the genetic factors related to PD?
Mutation in Parkin Gene Mutation in alpha-Synuclein gene
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What is the pathogenesis of PD?
- Neurodegenerative loss of dopamine secreting cells from the pars compacta of the substantia nigra that project to the striatum - Reduced striatal dopamine levels - Less dopamine means the thalamus will be inhibited resulting in a decrease in movement - symptoms of Parkinson’s - Under the microscope you will see the presence of intracytoplasmic intrusion bodies in the remaining neurones: Lewy bodies
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What are the typical Parkinsonism Symptoms?
Bradykinesia Resting Tremor Rigidity
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What are the symptoms of PD?
Parkinsonism (bradykinesia, Resting Tremor, Rigidity) Postural Instability Anosmia - early sign Constipation Sleep disturbances Cognitive/memory problems Depression
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What are the clinical signs of PD?
Signs are often Asymmetrical (unilateral) Pin rolling tremor of thumb Lead pipe arm (reduced arm swing) Shuffling gait Cogwheel movement
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What makes up a diagnosis of PD?
Clinical Dx based on Sx and Examination and Hx - Bradykinesia + 1 or more other Cardinal Sx DaTSCAN - Imaging to dopaminergic terminals in Str MRI/Head CT - may show SNpc Atrophy
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What is the treatment for PD?
No cure so Sx management - Levodopa (synthetic Dopamine) to increase levels (as dopamine cannot cross BBB) + Benserazide or Carbidopa - Dopa Decarboxylase inhibitors (eg. Carledopa (Levodopa + Carbidopa)) - Dopamine Agonists - Bromocriptine - COMT/MAO-B Inhibitors - Rasagiline (COMT) / Selegiline (MAO-B) Surgical - Deep Brain Stimulation
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What is the issue with using levodopa to treat PD?
Initially works well but soon the Px becomes resistant to it and the effects wear off. Therefore want to only use it when Sx are bad enough to prevent early resistance.
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What is an important differential diagnosis to PD?
Lewy body dementia (often associated with parkinsonism) Parkinson Sx then Dementia = Parkinson dementia Dementia then Parkinson Sx = Lewy body dementia w/ Parkinsonsim.
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What is dementia?
A syndrome caused by neurodegeneration of various causes resulting in progressive reduction of cognition and difficulty with ADLs
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What is the epidemiology of dementia?
Rare under 55 years Prevalence rises with age Alzheimer’s most common – more common in females Vascular and mixed dementias are more common in males Autosomal dominant – 10-20% of developing it
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What is the commonest cause of dementia?
Alzheimer's Disease (AD) Accounts for 60-75% of all dementias
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What is the epidemiology of AD?
Rarely affects under 65yrs (otherwise EOAD which accounts for 3% of cases) Affects more females than males Prevalence significantly rises with age
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What is the pathophysiology of AD?
Accumulation of Beta amyloid plaques (Ab plaques) and Tau Neurofibrillary tangles (NFT) in the cerebral cortex. This leads to cortical scarring and brain atrophy Additionally, damage to ACh neurons leading to poor neurotransmission
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What is the APP protein?
Amyloid Precursor protein that is pathologically cleaved into Beta Amyloid plaques that accumulate in the brain (AD) and other tissues (in amyloidosis)
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What are the risk factors for AD?
Increasing age Downs Syndrome APP gene mutation APOE4 allele for familial AD (linked to EOAD)
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What are the symptoms of AD?
Agnosia - cant recognise things Apraxia - Cant do basic motor skills Aphasia - Speech difficulties Amnesia - Memory impairment
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What is the progression of cognitive decline like in AD?
Steady progressive decline
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What is the second most common cause of dementia?
Vascular Dementia Accounts for roughly 20% of cases
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What is Vascular Dementia?
Cognitive decline that occurs in a stepwise manner due to a Hx of cerebrovascular events.
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What is the pathophysiology of Vascular dementia?
Hx of cerebrovascular events leads to infarction and loss of brain cells/damaged tissue. Neurons cannot regenerate so the neurodegeneration is permanent. Increased risk of secondary cerebrovascular events can lead to further brain damage and cognitive decline.
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What are the symptoms of vascular dementia?
Signs of vascular pathology: Raised BP Hx of cerebrovascular events Focal CNS signs General cognitive decline in a stepwise manner
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What is Lewy Body Dementia?
3rd most common form of dementia Alpha-Synuclein and Ubiquiting aggregates accumulate in the cerebral cortex Results in cognitive decline.
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What are the symptoms of Lewy Body Dementia?
Cognitive decline + Parkinsonism
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What is Frontotemporal dementia?
An uncommon form of dementia (5% of cases) Specific degeneration of frontotemporal lobes often causing speech and language deterioration and Thinking/memory problems
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What are the risk factors for Frontotemporal dementia?
FHx Autosomal dominant mutation in Tau protein (chromosome 17) FHx of MND (TDP-43)
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What is the Diagnostic test for dementia?
Mini Mental State Exam (MMSE) /30 >25 = normal 18-25 = impaired <17 = severely impaired Brain MRI - May show cortical atrophy
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What is the treatment for dementia?
Mostly Conservative: Social stimulation/interaction Exercise and healthier lifestyle
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What pharmacological treatment can be given to aid Alzheimer's Disease?
Sx management: First line: AChE inhibitors (rivastigmine, neostigmine) NMDA antagonist - memantine SSRIs - treat BPSD (behaviour and psychological Sx of dementia)
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What Pharmacological therapy can be given to aid vascular dementia?
Antihypertensives - Ramipril To reduce risk of subsequent cerebrovascular events Control CVD risk factors
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What are the primary headaches?
No underlying cause relevant to headache: Migraine Cluster Tension (Trigeminal Neuralgia)
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What are the secondary Headaches?
Due to underlying conditions: GCA Infection SAH Trauma Cerebrovascular disease Eye, Ear Sinus pathology Drug overdose
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Define a Migraine?
Recurrent throbbing headache often preceded by an aura and associated with nausea, vomiting and visual changes
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What is the epidemiology of a Migraine?
Most common cause of episodic (recurrent) headaches More common in females 90% onset in under 40 yrs (if onset > 50 yrs then think pathological)
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What happens to Migraine severity with age?
Severity of Migraine typically decreases with advancing age
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What are the potential triggers of a migraine?
CHOCOLATE: - Chocolate - Hangovers - Orgasms - Cheese - Oral contraceptives - Lie-ins - Alcohol - Tumult - loud noise - Exercise
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What are the different Types of migraine?
Migraine without aura Migraine with aura Silent migraine (migraine with aura but without a headache) Hemiplegic migraine
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What is the typical progression of migraines?
Occur in attacks that tend to follow a typical pattern: Prodrome Aura Throbbing headache Resolution Post-dromal/recovery
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Explain the progression of a Migraine?
Prodrome: Days prior to attack Mood changes Aura: last for 60mins Vision changes minutes before attack (attack follows soon after) ZigZag lines Throbbing Headache: 4-72hrs (Hemiplegic in some cases) Resolution: Headache fades away slowly Recovery
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What is the Clinical Dx of a migraine?
2 or more of: Unilateral pain Throbbing Motion Sickness Mood severely intense PLUS 1 or more of: Nausea Vomiting Photophobia/Phonophobia W/ A NORMAL NEURO EXAM
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What is the diagnostic criteria for a Migraine without Aura?
4 diagnostic criteria (ABCD): A – 5 attacks fulfilling B-D B - attacks last 4-72 hours C – two of the following Unilateral Pulsing Moderate/severe Aggravated by routine physical activity D – during headache at least one of Nausea and/or vomiting Photophobia (light sensitive) and phonophobia (sound sensitive)
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What is the Diagnostic Criteria for a Migraine with an Aura?
3 diagnostic criteria (ABC): A – at least 2 attacks fulfilling B and C B - > 1 reversible aura symptom Visual – zigzags, spots Unilateral sensory – tingling, numbness Speech – aphasia Motor weakness – known as “hemiplegic migraine” so rule out stroke and TIA C > 2 of the following 4 > 1 aura symptoms spread gradually over 5 minutes and/or > 2 aura symptoms occurring in successions Each aura symptom lasts 5-60 minutes > 1 aura symptom is unilateral Aura accompanied/followed within 60 minutes by headache
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How are migraines diagnosed?
Clinical Dx unless pathology is suspected where you do tests to exclude DDx: Neuro imaging LP
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What are the treatments for Migraines?
Conservative - Avoid Triggers Acute Mx: Mild - Paracetamol/NSAIDs - ibuprofen Severe - Triptans - sumatriptan Anti-emetics - metoclopramide Prophylaxis: 1st line – Propranolol (beta-blocker) or Topiramate (anti-convulsant) 2nd line – acupuncture 3rd line – Amitriptyline (tricyclic anti-depressant) 4th line – Botulinum toxin type A (only if not responded to 3 prior Tx)
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What is the mechanism of action of Triptans? Why are they used for migraines?
5-HT receptor agonists (serotonin) that are used to abort migraines when they start to develop
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What are cluster headaches?
Severe unilateral headaches often periorbital that come in clusters of attacks
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How long can a cluster headache last for?
Clusters of attacks may last for weeks/months before a pain free period follows which may last for years
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What is the primary feature of a cluster headache?
Periorbital unilateral pain Extremely painful (most disabling of primary headaches)
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Who typically presents with Cluster headaches?
Males 30-50 yrs old
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What are the risk factors for cluster headaches?
Male Smokers 30-50yrs old Genetics (autosomal dominant link)
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What are the types of Cluster headaches?
Episodic - > 2 cluster periods lasting 7 days to 1 year separated by pain free periods lasting > 1 month Chronic – attack occur for > 1 year without remission or with remission lasting <1 month
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What is the presentation of cluster headaches?
- Cluster headache – can take 3 years to get a diagnosis - A – At least 5 headache attacks fulfilling B-D - B – Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 minutes if untreated and rises to crescendo - C – headache is accompanied by ipsilateral cranial autonomic features and/or sense of restlessness or agitation - D – attacks have a frequency from 1 every other day to 8 per day Deemed to have a boring/hot poker characteristic - Associated with ipsilateral eye lacrimation and redness, rhinorrhoea (blocked nose), miosis (excessive pupil constriction) and/or ptosis (drooping or falling of upper eyelid) - Usually occur in middle of the night or morning hours
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What is the diagnosis of cluster headaches?
Clinical Dx 5 or more similar attacks fulfilling criteria
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What is the treatment of cluster headaches?
Acute Mx: Triptans - SC Sumatriptan or IM Zolmitriptan High flow 100% oxygen Prophylaxis: Verapamil (CCB)
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What are Tension Headaches?
The most common form of a primary headache which has a characteristic rubber band feeling around the head.
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What is the Epidemiology of Tension headaches?
Most common primary headache Can be episodic (<15 days/month) or chronic (>15 days a month for at least 3 months)
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What are the causes of Tension Headaches?
Neurovascular irritation which refers to scalp muscles and soft tissues MC SCOLD: Missed meals Conflict Stress Clenched jaw Overexertion Lack of sleep Depression
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What is the Presentation of a Tension headache?
- A - > 10 attacks occurring <1 day/month (<12 days/year) and fulfilling B-D - B - Headache lasting from 30 minutes to 7 days - C – headache has two of the following Bilateral Pressing/tightening (non-pulsatile) quality Mild or moderate intensity/pain Not aggravated by routine physical activity (e.g. walking or climbing stairs) - D – both of the following No nausea or vomiting (anorexia may occur) No more than one of photophobia and phonophobia - E – not attributed to another disorder
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What is the diagnosis for a tension headache?
Clinical Diagnosis from Hx
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What is the treatment for a Tension headache?
Stress relief Avoid triggers Simple analgesia: Aspirin/Paracetamol
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What is the main risk factor/trigger for a tension headache?
STRESS
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What is Trigeminal Neuralgia?
A chronic, debilitating condition resulting in intense and extreme episodes of pain
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What are the risk factors for Trigeminal Neuralgia?
Increased age MS Female HTN
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What is the Epidemiology of Trigeminal Neuralgia?
Females 50-60 yrs Increases with age Almost always Unilateral
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What are the causes of Trigeminal Neuralgia?
Compression of the trigeminal Nerve that leads to excitation and erratic pain: - Vein or artery compressing CN5 - Local Pathology pressing on CN5 (tumours/Aneurysms) - CN5 nerve lesion
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What is the headache like in Trigeminal Neuralgia?
Electric Shock Pain that lasts for seconds to minutes across the face 90% unilateral 10% bilateral
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What is the diagnostic criteria for trigeminal neuralgia?
Clinical Dx 3 or more attacks with characteristic unilateral facial pain and Symptoms MRI - exclude secondary causes/other pathology
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What are the treatment options for trigeminal neuralgia?
First Line: Carbamazepine (anticonvulsant) Second Line: Phenytoin/Gabapentin (analgesic targeted for neuropathic pain) Surgery possible to decompress/intentionally damage nerve
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Overview of Primary Headache Features: Duration Site Character Severity Acute Tx
Duration: MH - 4-72 hrs TH - Minutes to dates CH - 15-180 mins TGN - Few seconds Site: MH - Unilateral TH - Bilateral CH - Retro-orbital/unilateral TGN - unilateral V1/2/3 distribution Character: MH - Throbbing TH - Pressing/tight band CH - Hot poker/boring TGN - Electric shock/stabbing Severity: MH - Moderate-severe TH - Mild to moderate CH - Severe to very severe TGN - Severe to very severe Acute Tx: MH - Triptan TH - Paracetamol CH - Triptan/100% O2 TGN - Carbamazepine
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Define a Seizure?
A paroxysmal alteration of neurological function as a result of excessive, hypersynchronous discharge of neurons within the brain
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Define Epilepsy?
A neurological disorder characterised by an increased tendency to have recurrent seizures that are idiopathic and unprovoked. (>2 episodes more than 24hrs apart)
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What are the different causes of seizures?
VITAMIN DE: Vascular Infection Trauma Autoimmune - SLE Metabolic - Hypocalcaemia Idiopathic - Epilepsy Neoplasms Dementia + Drugs (cocaine) Eclampsia + everything else
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What are the risk factors for developing epilepsy?
Familial inherited Dementia (10x more likely) Drug use Cerebrovascular events
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What is the epidemiology of epilepsy?
One of the most common neurological disorders 2% of UK population will have 2 or more seizures Highest prevalence at extremes of life (<20yr or >60yrs)
272
What is the pathophysiology of seizures?
Disrupted neurological function resulting in an imbalance between inhibition and excitation of neurons. Balance of GABA and Glutamate shifts towards glutamate Therefore more excitatory stimulation
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What are the different types of seizures?
Epileptic vs Non-Epileptic: Generalised Focal
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Define an Epileptic Seizure
Paroxysmal event in which changes of behaviour, sensation or cognitive processes are caused by excessive (too much voltage), hypersynchronous neuronal discharges in the brain
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What are the characteristics of an epileptic seizure?
Duration – 30-120 seconds Positive ictal symptoms – excess of something Seeing/hearing something that isn’t there Feeling touch when you aren’t being touched Negative postictal symptoms May occur from sleep May be associated with other brain dysfunction – bleeds, stroke, tumours etc. Typical seizure phenomena – lateral tongue bite, déjà v
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Define a Non-Epileptic Seizure?
Paroxysmal event in which changes in behaviour, sensation and cognitive function caused by mental processes associated with psychosocial distress
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What are the characteristics of a Non-epileptic Seizure?
Situational Duration 1 – 20 mins Dramatic motor phenomena or prolonged atonia Eyes closed Ictal crying and speaking Surprisingly rapid or slow postictal recovery History of psychiatric illness, other somatoform disorders
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What are the subtypes of generalised seizures?
Tonic Clonic Absence Toni Myoclonic Atonic
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What are the subtypes of Focal Seizures?
Simple focal complex focal
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How are Seizures classified?
Where the seizures began Level of awareness during the seizure Other features of the seizure e.g. motor
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What are generalised seizures?
A seizure that starts within both hemispheres of the brain at onset. They are bilateral ALWAYS a loss of consciousness
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What are Focal Seizures?
Seizures that originate within one side of the brain and are usually confined to one region. They may progress to secondary lobes (Focal-bilateral seizures)
283
What is the clinical progression of an epileptic seizure?
Prodrome: (days before) Mood changes Pre-Ictal: (minutes before) Aura Seizure trigger Automatisms - lip smacking/rapid blinking Ictal Event: The Seizure Post-Ictal Period: (30 mins after) Headaches Confusion / reduced GCS Todd's Paralysis Amnesia Sore tongue
284
What are the features of a Tonic Clonic seizure?
No aura Loss of consciousness Tonic phase - rigidity/muscle tensing (fall to floor) Clonic phase - Jerking of limbs/muscles Upgazing open eyes Incontinence Tongue bitten
285
What is the management of a Tonic Clonic Seizure?
First line: sodium valproate Second line: lamotrigine or carbamazepine
286
What is an Absence Seizure?
Typically in children: Px stares blankly into space (seconds to mins) Unaware of surrounds and will not respond. Will then carry on as normal after the seizure.
287
What is a tonic seizure?
A seizure where there is just rigidity/muscle tensing
288
What is a Myoclonic seizure?
A seizure where there is just jerking limbs
289
What is an Atonic Seizure?
Sudden floppy limbs and muscles They may be indicative of Lennox-Gastaut syndrome
290
What is a febrile convulsion?
Seizures that occur in children whilst they have a fever. They are not caused by epilepsy or underlying pathology.
291
What parts of the brain are affected in a generalised Seizure?
All the cortex and deep brain structures bilaterally affected.
292
What parts of the brain are affected in a simple focal seizure?
The Focal region of cortex NO basal ganglia/thalamus involvement
293
What parts of the brain are affected in a complex focal seizure?
The focal region of cortex Basal ganglia and thalamus are involved.
294
What is a Simple Focal Seizure?
No Loss of consciousness The patient is awake and aware Will have uncontrollable muscle jerking and may be unable to speak
295
What is a Complex Focal Seizure?
There is loss of Consciousness Patient is unaware
296
What are the symptoms of Focal seizures?
Dependent on where the focal deficit is located
297
What is the most common region affected in a focal seizure?
Temporal lobe
298
What are the features of a Temporal focal seizure?
Oral automatism: lip smacking, chewing, swallowing Manual automatisms: picking, fumbling Automatic behaviour: running, walking Auras: déjà vu, feeling of fear, unpleasant smells Auditory: buzzing, ringing, vertigo
299
What are the features of a Frontal focal seizure?
Predominantly motor symptoms: pelvic thrusting, bicycling, tonic posturing Sexual automatisms Bizarre behaviour Vocalisations
300
What are the features of a Parietal focal seizure?
Parasthesias Visual hallucinations Visual illusions More subjective and difficult to diagnose than other areas
301
What are the features of a Occipital focal seizure?
Visual hallucinations Transient blindness Rapid and forced blinking Movement of head or eyes to the opposite side
302
What is required for a diagnosis of Epilepsy?
Must have had 2 or more seizures MORE THAN 24 hrs apart to be considered: CT/MRI head - Examine HIPPOCAMPUS, check for bleeds and trauma EEG: 3H2 wave in absence Bloods: rule out metabolic/infection
303
What is the Treatment for epilepsy and seizures?
Sodium Valporate for generalised epilepsy Carbamazepine for focal seizures Surgical resection possible
304
What is a contraindication for using Sodium Valporate?
All females of childbearing age (15-45) Sodium Valporate is Teratogenic Instead use Lamotrigine
305
What is a complication of Epilepsy?
Status Epilepticus (NEURO EMERGENCY) Epileptic seizures without a break back to back OR Seizure lasting >5 minutes
306
What are the symptoms of STATUS EPILEPTICUS?
Post ictal confusion Todd’s palsy – paralysis in arms or leg (usually isolated to one side of the body Can last ~15 hours and usually subsides in around ~2 days Temporary and severe suppression of seizure-affected area
307
What is the treatment for Status Epilepticus?
Benzodiazepines: Lorazepam 4mg IV If not worked then Lorazepam again. Then Phenytoin if second dose doesnt work.
308
What are the differences between an epileptic and non-epileptic seizure?
Epileptic Seizures have: Eyes OPEN Synchronous Movements Can occur in sleep
309
What must you do if you are diagnosed with Seizures?
Inform DVLA Cannot drive until seizure free for one year
310
What is the length of the spinal cord?
From C1-L1/2
311
Where is the conus medullaris and cauda equina?
At L1/2
312
Define Hemiplegia?
Paralysis to one side of the body (usually due to a brain lesion)
313
Define Paraplegia?
Paralysis of both legs/lower body (usually due to a spinal cord lesion)
314
What does the DCML tract convey information for?
Ascending tract for fine touch, 2pt discrimination and proprioception.
315
What is the pathway for the DCML
Travels in dorsal route (Fasciculus Gracilis/Cuneatus) Decussates in the medulla
316
What does the spinothalamic tract convey information for?
Ventral: Crude Touch and pressure Lateral: Pain and temperature
317
What is the pathway for the spinothalamic tract?
Ascending: Enters at spinal level of nerve ascends 1-2 spinal levels and then decussates
318
What information does the corticospinal tract convey?
Upper motor neurons for movement. Decussates at the medulla
319
What are the nerve routes for the Knee jerk reflex?
L3/4
320
What are the nerve routes for the Big toe reflex?
L5
321
What are the nerve routes for the ankle Jerk reflex?
S1/2
322
What are the commonest causes of spinal cord injury?
Trauma Vertebral compression fractures Intervertebral disc disease - prolapse/herniation Tumours Infection
323
What are the common vertebral body neoplasms that can cause spinal compression?
Mets from: Lungs Breast RCC Melanoma
324
What are the different types of spinal cord injury?
Complete SC injury Anterior SC injury Posterior SC injury Central SC injury Brown-Sequard Syndrome
325
What is Spinal Cord Compression?
Compression of the spinal cord resulting in upper neurone signs and specific symptoms dependent on where compression is
326
What is the commonest cause of acute spinal cord compression?
Vertebral body neoplasms
327
What are the main causes of Spinal Cord Compression (myelopathy)?
Tumour (slow onset) Osteophytes Disc prolapse (slower onset) Nucleus pulposus moves and presses against the annulus but it doesn’t escape outside the annulus Can produce a bulge in the disc which, sometimes, can result in pressure (less pressure than herniation) on nerve root resulting in pain Disc herniation - centre of disc (nucleus pulposus) has moved out through the annulus (outer part of disc) resulting in pressure on nerve root and pain
328
What are the symptoms of spinal cord compression?
Sx depend on level of cord compression: UMN signs below level of lesion – everything goes up Sensory loss below level of lesion LMN signs AT level Bladder sphincter involvement – hesitancy, frequency, painless retention
329
What is the concern if there is sphincter involvement in spinal cord compression
This is a late and bad sign signalling a poorer prognosis
330
What would be the features of a complete spinal cord compression?
All motor and sensory function below the SCI level
331
What would be the features of an anterior spinal cord compression?
Disruption of anterior spinal cord or anterior spinal artery Loss of motor function below the level Loss of pain and temperature sensation (anterior column) Preservation of fine touch and proprioception (posterior column)
332
What would be the features of a posterior spinal cord compression?
Disruption of posterior spinal cord or posterior spinal artery (rare) Loss of fine touch and proprioception (posterior column) Preservation of pain and temperature sensation (anterior column)
333
What are some differential Diagnoses for Spinal Cord Compression?
Transverse myelitis MS Cord vasculitis Trauma Dissecting aneurysm
334
What is the primary investigation if suspecting a Spinal cord compression?
MRI Spinal cord ASAP: (risk of permanent damage) CT CAP - if malignancy suspected + biopsy to identify nature
335
What is the treatment for spinal cord compression?
Neurosurgery to decompress cord Dexamethasone to reduce inflammation
336
What is Brown Sequard Syndrome?
Hemi-section of the spinal cord and therefore loss of sensations of pain temperature and touch and motor movement
337
What are the causes of Brown-Sequard Syndrome?
Space occupying lesions Intervertebral disc prolapses Vertebral bone fractures Trauma – gunshot wounds, knife wounds Infectious – HIV MS
338
What would be the clinical features of brown-Sequard syndrome?
- (Ipsilateral Corticospinal) Ipsilateral weakness and loss of motor function below the lesion. - (Ipsilateral DCML) Ipsilateral loss of proprioception, 2-point discrimination and fine touch. - (Contralateral Spinothalamic) Contralateral loss of pain and temperature sensation 1-2 spinal segments below the lesion.
339
What is the Investigation and Treatment for Brown Sequard Syndrome?
Ix - MRI Spine Tx - Supportive (physical/occupational therapy) and Steroids (Dexamethasone)
340
What is Sciatica?
Sciatica refers to the symptoms associated with irritation of the sciatic nerve.
341
What spinal nerves form the sciatic nerve? Where is the most common region of compression to cause Sciatica?
L4-S3 spinal roots Most common region of compression at L5/S1
342
What is the innervation of the sciatic nerve?
The sciatic nerve supplies sensation to the lateral lower leg and the foot. It supplies motor function to the posterior thigh, lower leg and foot.
343
What nerves are branches of the sciatic nerve?
Common peroneal nerve Tibial nerve
344
What are the symptoms of Sciatica?
- Unilateral pain from the buttock radiating down the back of the thigh to below the knee or feet - Paraesthesia (pins and needles), numbness and motor weakness - Reflexes may be affected depending on spinal root affected Signs: Unilateral Weak plantar flexion Absent right ankle jerk Decreased sensation over lateral edge and sole of right foot
345
What are the main causes of Sciatica?
Intervertebral Herniated/prolapsed disc Tumours Piriformis Syndrome Spondylolisthesis Spinal stenosis
346
What is Bilateral sciatica a red flag for?
Cauda Equina syndrome
347
What is the Socrates mnemonic for?
Assessing pain S – Site O – Onset C – Character R – Radiation A – Associations T – Timing E – Exacerbating and relieving factors S – Severity
348
What are the diagnostic investigations for sciatica?
Clinical Dx generally: Can't Do straight leg raise test without pain May have: XR CT MRI - if cauda equina suspected
349
What is the main treatment for sciatica?
Physiotherapy + Analgesia: Amitriptyline Duloxetine
350
What is Cauda Equina Syndrome (CES)?
Surgical emergency where the nerve roots of the cauda equina at the bottom of the spine are compressed below the conus medullaris (L2)
351
What do the nerves of the cauda equina supply?
Sensation to the lower limbs, perineum, bladder and rectum Motor innervation to the lower limbs and the anal and urethral sphincters Parasympathetic innervation of the bladder and rectum
352
What are the main causes of CES?
Large Central Herniated disc (the most common cause) Tumours, particularly metastasis Spondylolisthesis (anterior displacement of a vertebra out of line with the one below) Abscess (infection) Trauma
353
What is the most common cause of CES?
Lumber Herniation L4/5 or L5/S1
354
What are the main symptoms of CES?
Leg weakness w/ LMN signs (ipsilateral hypotonia, fasciculations, hyporeflexia) Saddle anaesthesia - perianal numbmess Bladder/Bowel dysfunction + sphincter involvement Erectile Dysfunction
355
What are the main Signs of CES?
Areflexia Fasciculations Loss of bowel/bladder control Urinary retention
356
What is the diagnostic investigation for CES?
MRI spinal cord (diagnostic) Testing nerve roots/reflexes
357
What is the treatment for CES?
Refer to neurosurgeon ASAP to relive pressure Surgical decompression High dose dexamethasone Corticosteroids
358
What are the red flag signs in CES?
Bilateral sciatica Bilateral flaccid leg weakness Saddle anaesthesia Bladder and bowel dysfunction Erectile dysfunction Areflexia
359
What is the main difference between CES and spinal cord lesions above the CE?
Major difference between cauda equina and lesions higher up in the cord is that leg weakness is flaccid and areflexic (LMN lesion) and not spastic and hyperreflexic (UMN lesion)
360
Where do the cranial Nerves arise from?
CN1 - Olfactory Bulb CN2 - Optic Chiasm CN3 - Interpeduncular fossa CN4 - Dorsal aspect of Midbrain CN5 - Lateral Pons CN6 - Pontomedullary Junction CN7 - Pontomedullary Junction CN8 - Pontomedullary Junction CN9 - Medulla CN10 - Medulla CN11 - Medulla (below CN12) CN12 - Medulla (Above CN11)
361
What is the causes of Cranial nerve lesions?
Damage to the brainstem: - Tumour - MS - Trauma - Aneurysm - Vertebral artery dissection resulting in infarction - Infection - cerebellar abscess from ear
362
What are the Symptoms of a CN1 Palsy?
Anosmia - Cant smell
363
What are the Symptoms of a CN2 Palsy?
Loss of vision in the eye of optic nerve lesion
364
What are the symptoms of a CN3 palsy?
Ptosis Down and out eye Fixed and dilated pupil
365
Why do you get a down and out eye in a CN3 palsy?
Unopposed action of the Trochlear (CN4) and Abducens (CN6) cranial nerves
366
Why do you get a fixed and dilated pupil in a CN3 palsy?
Loss of parasympathetic outflow from the Edinger-Westphal nucleus supplying the pupillary sphincter and ciliary bodies.
367
What are the causes of a CN3 palsy?
* Raised ICP * Diabetes * Hypertension * Giant cell arteritis
368
What are the symptoms of a CN4 palsy?
Diplopia (double vision) when looking down "walking down stairs"
369
What are the causes of a CN4 palsy?
Rare: Due to trauma of the orbit
370
What are the symptoms of a CN5 palsy?
- Jaw deviates to side of lesion - Loss of corneal reflex
371
What are the causes of a CN5 Palsy?
Trigeminal Neuralgia (pain but no sensory loss) VZV nasopharyngeal cancer
372
What are the symptoms of a CN6 palsy?
Adducted eye
373
What are the causes of a CN6 palsy?
Raised ICP MS Wernicke's Encephalopathy Pontine Stroke
374
What are the symptoms of a combined CN3,4,6 palsy?
Non-Functional Eye
375
What are the causes of a combined CN3,4,6 palsy?
* Pontine Stroke * Tumours * Wernicke’s encephalopathy
376
What are the signs of a CN7 palsy?
unilateral facial weakness (motor component), altered taste (sensory component), and a dry mouth (parasympathetic component).
377
What are the causes of a CN7 palsy?
Bells Palsy Fractures to pteroid bone Parotic inflammation Otitis Media
378
What is Bells Palsy?
Neurological condition that presents with a rapid onset of unilateral facial paralysis
379
What is clinically relevant about the control of the facial muscles?
The lower half of the faces only has contralateral innervation Top half has bilateral. forehead sparing
380
How can you tell if a bells palsy is an UMN or LMN lesion?
UMN injured, lower half on contralateral side is weak but forehead is not as it has contralateral and ipsilateral innervation (bilateral) LMN - weakness of all the muscles on the ipsilateral side of the face
381
How do you determine the level of CN7 lesion?
Proximal to pons - loss of all function (lacrimation, salivation, taste, facial weakness) Lesion above chorda tympani (same as previous but does have lacrimation) Distal Lesion to the stylomastoid foramen (facial weakness only)
382
How do you determine the level of CN7 lesion?
Proximal to pons - loss of all function (lacrimation, salivation, taste, facial weakness) Lesion above chorda tympani (same as previous but does have lacrimation) Distal Lesion to the stylomastoid foramen (facial weakness only)
383
What are the symptoms of a CN8 palsy?
Hearing impairment Vertigo Loss of balance
384
What are the causes of a CN8 palsy?
Skull fracture Otitis Media Tumours Compression
385
What are the symptoms of a CN9 and CN10 palsy?
- Gag reflex issues - Swallowing issues - Vocal issues - hoarse voce
386
What are the causes of a CN9/CN10 palsy?
Jugular foramen lesion
387
What are the symptoms of a CN11 palsy?
Can't shrug shoulders/turn head against resistance
388
What are the symptoms of a CN12 palsy?
Tongue deviation towards the side of the lesion
389
Define Weakness/paresis
impaired ability to move a body part in response to will
390
Define Paralysis?
ability to move a body part in response to will is completely lost
391
Define Ataxia/
willed movements are clumsy, ill-directioned or uncontrolled (usually due to an issue with the cerebellum)
392
Define Apraxia?
disorder of consciously organised patterns of movement or impaired ability to recall acquired motor skills
393
What is a Motor Unit?
Basic functional unit of muscle activity Alpha motor neuron (LMN) + axon + skeletal muscle fibres it innervates Number of muscles fibres depends on sophistication of the movement e.g. hands and eyes (finely controlled), each motor neuron will only control a few muscle fibres whereas in bulky muscles, each motor neuron will supply more muscle fibres
394
What is the organisation of Movement?
Idea of movement – association areas of cortex Activation of upper motor neurons in the pre-central gyrus Impulses travel to lower motor neurons and their motor units via the corticospinal (pyramidal) tracts Modulating activity of the cerebellum and basal ganglia Hence why individuals with cerebellar and basal ganglia disorders can’t control movements properly Further modification of movement depending on sensory feedback
395
How is Muscle Tone Regulated?
Stretch receptors in muscle (muscle spindles) innervated by gamma motor neurons Muscle stretched 🡪 afferent impulses from muscle spindles which 🡪 reflex partial contraction of muscle Disease states e.g. spasticity and extrapyramidal rigidity alter muscle tone by altering the sensitivity of this reflex
396
What is Motor Neuron Disease (MND)
Progressive neurodegenerative disease where both upper and lower motor neurons stop functioning but there is no effect on the sensory neurons.
397
What is the most common form of MND?
Amyotrophic Lateral Sclerosis (ALS) Accounts for 50% of cases
398
What are the risk factors of MND?
Increased age >60 yrs Male FHx Smoking RUGBY
399
What genetic mutation is linked with MND?
SOD-1 mutation
400
What is the main motor tract in the body?
Corticospinal tract UMN from precentral gyrus Anterior (10% - no decussation) Lateral (90% - Decussation in Medullary pyramids)
401
What are the different types of MND?
Amyotrophic Lateral Sclerosis (ALS) Progressive Muscular Atrophy (PMA) Primary Lateral Sclerosis (PLS) Progressive Bulbar Palsy (PBP)
402
What is the Epidemiology of MND?
More common in men Most commonly affects people in middle age ALS - most common type of MND Most die within 3 years of diagnosis – usually from respiratory failure as a result of bulbar palsy and pneumonia
403
What are the signs of ALS?
UMN and LMN signs
404
What are the signs of PMA?
LMN only Has best prognosis
405
What are the signs of PLS?
UMN signs only
406
What are the signs of PBP?
CN9-12 affected Speech and swallowing issues Worst prognosis
407
What is the pathology of MND?
Degenerative condition affecting motor neurons – mainly the anterior horn cells There is relentless and UNEXPLAINED destruction of UMN and anterior horn cells in the brain and spinal cord Causes both UMN and LMN dysfunction UMN and LMN affected but no sensory or sphincter loss – distinguishes from MS Never affects eye movements – distinguishable from myasthenia gravis
408
What are the signs of an Upper motor neuron (UMN) lesion?
Hypertonia Rigidity + spasticity Hyperreflexia Babinski Reflex Positive - Big toe goes up when stroking foot Power: Arms - Flexors > Extensors Legs - Flexors < Extensors
409
What are the signs of a Lower Motor Neuron (LMN) Lesion?
Hypotonia Flaccidity + muscle wasting Hyporeflexia Fasciculations Babinski Reflex Negative - big toe goes down when stroking foot Generally loss of power
410
What should you think if you see a patient with mixed Upper and lower motor neuron signs?
MND!!
411
Where is an UMN lesion?
Anywhere on a motor nerve between the pre-central gyrus to the anterior spinal cord
412
Where is a LMN lesion?
Anywhere on a motor nerve between the anterior spinal cord and the innervated muscle
413
What is NEVER affected in MND?
Eye muscles: Affected in MS and MG Sensory Function and Sphincters: Affected in MS and Polyneuropathies
414
What are the symptoms of MND?
Progressive weakness Falls Speech and swallowing issues (in PBP)
415
What is split hand sign?
Disproportionate wasting of the thenar muscles compared to the hypothenar muscles
416
What are the clinical signs of MND?
Mixed UMN and LMN signs Dysarthria / Dysphagia Fasciculations Split Hand Sign
417
What is the primary investigation for MND?
Clinical Dx due to mixed UMN/LMN picture - LMN/UMN signs in 3 regions EMG - fibrillation potentials May carry out MRI / CSF examinations for exclusion of differentials
418
What are some good diagnostic tips to exclude DDx of MND?
No sensory loss = rules out MS or myelopathy No disturbances in eye movements = rules out Myasthenia Gravis or MS No sphincter disturbances = rules out MS
419
What is the management of MND?
No cure - progressive Supportive therapy: Physiotherapy Breathing support if needed Pharmacological Tx: Riluzole - anti-glutaminergic
420
What are the complications of MND?
Aspiration pneumonia Respiratory failure
421
What is Myasthenia Gravis (MG)?
Autoimmune condition characterised by Autoantibodies against the nicotinic Acetylcholine receptors (nAChR) at the neuromuscular Junction.
422
What type of Hypersensitivity reaction is Myasthenia Gravis?
Type 2
423
What are the risk factors for MG?
Females FHx Autoimmunity Thymoma/ Thymic Hyperplasia
424
What is the epidemiology of MG?
Generally more common in Females Female peak (20-30yrs) - associated with autoimmune disease Male peak (50-60yrs) - associated with Thymoma
425
What is the pathophysiology of MG?
85% Anti-nACh Receptors: - Bind to post synaptic receptor and competitively inhibit ACh binding. - ACh cannot bind during exertion and therefore there is progressive weakness of muscles - Auto-ABs Will also bind to complement factors and cause NMJ destruction 15% Anti MuSK: Inhibit MuSK from synthesising ACh Receptors so there is reduced expression on post synaptic membrane.
426
What are the symptoms of MG?
Lethargy Muscle weakness that starts at head/neck and moves downwards Weak eye muscles - diplopia Ptosis Jaw fatiguability - slurred speech/ chewing difficulties Swallowing difficult
427
What is the progression of weakness like in MG?
Worse during the day/with exertion Better with rest Due to more AChRs being required in exertion and therefore greater inhibiton
428
What are the clinical signs of MG?
ptosis Head drop Myasthenic Snarl - difficulty smiling
429
What is the primary investigation for MG?
Serology - Ab testing: Anti-nACh-R Abs (85%) Anti-MuSK Abs (15%) Bedside tests - Count to 50 and as they reach higher numbers their voice becomes less audible Nerve Stimulation Tests - decrement in evoked potential after motor nerve stimulation Edrophonium Test CT/MRI - look for Thymoma
430
What is the Edrophonium Test?
Give Edrophonium (neostigmine) and AChE inhibitor to increase ACh Will give brief/temporary relief of Sx and increase muscle power
431
What is the first line treatment for MG?
1st Line: Reversible AChE inhibitors: Rivastigmine, Neostigmine Pyridostigmine 2nd Line: Immunosuppressants Prednisolone/Azathioprine Potentially Monoclonal Abs (Rituximab)
432
What is the main complication of MG?
Myasthenic Crisis: Severe acute worsening of Sx Often Triggered by another illness (URTI) Severe Respiratory weakness
433
What is the Treatment for Myasthenic Crisis?
IV Ig (immunoglobulin) and Plasmapheresis Non-invasive ventilation: BiPAP for Resp failure
434
What is a differential Diagnosis of Myasthenia Gravis?
Lambert Eaton Syndrome
435
What is Lambert Eaton Syndrome?
A NMJ syndrome which has similar Sx to MG. Autoimmunity against VG-Ca channels thereby reducing ACh release at the NMJ causing muscle weakness.
436
What is the cause of Lambert Eaton Syndrome?
Unclear but likely a paraneoplastic syndrome: Typically occurs in Px with Small Cell Lung Cancer (SCLC)
437
What is the presentation of Lambert Eaton Syndrome?
Proximal muscle weakness that develops more slowly Sx start at extremities and progress towards the head Shares most of same Sx with MG
438
What is the difference between MG and Lambert Eaton Syndrome clinically?
Lambert Eaton Syndrome symptoms tend to improve following a period of strong muscle contraction. Post Tetanic Potentiation
439
What is the Treatment for Lambert Eaton Syndrome?
Dx and Tx underlying condition (often SCLC) Amifampridine - blocks K+ channels and increases ACh release + Steroids and Immunosuppressants
440
What is Syncope?
Transient loss of consciousness due to transient global reduction in cerebral perfusion with complete and rapid recovery
441
What are the classifications of the causes of syncope?
Neurally mediated: Vasovagal Orthostatic (postural) syncope Cardiac syncope Structural Arrythmias
442
What is vasovagal syncope?
Vagus nerve receives a strong signal: Emotion, pain, temperature change Activates Parasympathetic NS Dilates blood vessels reducing cerebral perfusion causing hypoperfusion of the brain leading to collapse
443
What is the prodrome of syncope (presyncope Symptoms)?
Hot or clammy Sweaty Heavy Dizzy or lightheaded Vision going blurry or dark Headache
444
What are the causes of primary syncope?
Dehydration Missed meals Extended standing in a warm environment, such as a school assembly A vasovagal response to a stimuli, such as sudden surprise, pain or the sight of blood
445
What are the causes of secondary syncope?
Hypoglycaemia Dehydration Anaemia Infection Anaphylaxis Arrhythmias Valvular heart disease Hypertrophic obstructive cardiomyopathy
446
What is Orthostatic syncope?
Syncope due to postural change (standing from sitting) Occurs due to: Upon standing blood pools in the lower limbs/lower abdomen → venous return decreases → transient ↓cardiac output Sympathetic activation increases SV. reduction of Parasympathetic stimulation further increases HR and CO. Failure of these mechanisms leads to orthostatic syncope
447
What are the classical characteristics of syncope?
Situational Typically, from sitting or standing Rarely from sleep Presyncopal symptoms Occipital – see stars, dizzy and light headed, vision goes black Temporal – noises may sound distorted Back of brain most sensitive to oxygen Duration – 5-30 seconds Recovery within 30 seconds Cardiogenic syncope – less warning, history of heart disease
448
What are the primary investigations for syncope?
Clinical Hx and examination Ix to rule out pathological causes: Bloods - infection FBC - anaemia ECG- arrythmia Glucose - Hypoglycaemia B-hCG - ectopic pregnancy
449
What is the management of Syncope?
Confirm Dx to exclude underlying pathology Avoid Dehydration Avoid missing meals Avoid standing still
450
What are the different functions of the different nerve fibre types?
A-alpha – proprioception A-beta – light touch, pressure, vibration A – delta – dull pain and cold C – fibres – sharp pain and warmth
451
What is a mononeuropathy?
A process of nerve damage that affects a single nerve
452
What is polyneuropathy?
Disorders of peripheral or cranial nerves, whose distribution is usually symmetrical and widespread (multi-systemic) Often due to: Diabetes MS Guillain Barre
453
What is Mononeuritis Multiplex?
A type of peripheral neuropathy where there is damage to several individual nerves due to systemic causes.
454
What are the causes of Mononeuritis Multiplex?
WARDS PLC: - Wegener’s granulomatosis - Aids/Amyloid - Rheumatoid arthritis - Diabetes mellitus - Sarcoidosis - Polyarteritis nodosa - Leprosy - Carcinoma
455
What is Peripheral Neuropathy? What are the types of peripheral nerve disease?
Nerve pathology outside of the CNS that affects the peripheral nerves Mononeuropathy Polyneuropathy
456
What are some causes of peripheral nerve disease?
DAVIDE: Diabetes Alcohol Vitamin B12 Deficiency Infective/malignant Drugs - isoniazid Every vasculitis
457
What are the mechanisms of Peripheral Neuropathy?
Demyelination Axonal Damage - Nerve cut Nerve Compression Vasa Nervorum Infarction Wallerian Degeneration (Nerve lesion and distal end dies)
458
What are the 6 mechanisms of peripheral neuropathy and how do they occur?
- Demyelination o Schwann cell damage leads to myelin sheath disruption o Results in marked slowing of conduction e.g. in Guillain Barre syndrome - Axonal degeneration o Axonal damage causes the nerve fibre to die back from periphery o Conduction velocity initially remains mortal because axonal continuity is maintained in surviving fibres o Axonal degeneration occurs in toxic neuropathies - Compression o Focal demyelination at the point of compression causes disruption of conduction o Typically occurs in entrapment neuropathies e.g. carpal tunnel syndrome - Infarction o Micro-infarction of vasa nervorum occurs in diabetes and arteritis such as polyarteritis nodosa and eosinophilic granulomatosis with polyangiitis (GPA) - Infiltration o Infiltration occurs by inflammatory cells in leprosy and granulomas such as sarcoid and by neoplastic cells (cancer) - Wallerian degeneration o Process that results when a nerve fibre is cut or crash and the distal part of the axon that is separated from the neuron’s body degenerates
459
Give some examples of Mononeuropathies
- Carpal tunnel syndrome (medial nerve) – most common - Ulnar neuropathy (entrapment at the cubital tunnel) - Peroneal neuropathy (entrapment at the fibular head) - Cranial mononeuropathies (III or VII cranial nerve palsy) Idiopathic Immune mediated Ischaemic
460
What are the investigations for a peripheral neuropathy?
- History - Clinical examination Reduced or absent tendon reflexes Sensory deficit Weakness – muscle atrophies - Neurophysiological examination i.e. Nerve conduction studies/QST Demyelinating 🡪 Slow conduction velocities Axonal 🡪 Reduced amplitudes of the potential
461
What is the management for peripheral neuropathy?
Symptomatic Tx: Pain – give anti-neuralgic (GAP) - Gabapentin, Amitriptyline, Pregabalin Cramps - Quinine Balance - Physiotherapy/walking aids Aim is to identify any reversible cause and stop disease progression if possible
462
What is the most common Mononeuropathy?
Carpal Tunnel Syndrome
463
What is the pathophysiology of Carpal Tunnel Syndrome?
Compression/pressure of the Median Nerve as it passes through the Flexor Retinaculum "carpal tunnel"
464
What are the causes of Carpal Tunnel Syndrome?
Mostly Idiopathic Also: (HODPARAR) Hypothyroidism Obesity Diabetes Pregnancy Acromegaly Rheumatoid Arthritis Amyloidosis Repetitive Strain Injury
465
Who is more likely affected by Carpal Tunnel Syndrome?
Females due to narrower wrists so more likely to have compression Over 30s
466
What is the presentation of Carpal Tunnel Syndrome?
Gradual Onset of Sx Start off as intermittent Sx Worse at night
467
What are the Symptoms of Carpal Tunnel Syndrome?
Sensory Symptoms: Palmer aspects and full fingertips of: Thumb Index and middle finger The lateral half of ring finger Motor Symptoms: Thenar Muscles Flexor Pollicis Brevis Abductor Pollicis Opponens Pollicis
468
What are the sensory symptoms of Carpal Tunnel Syndrome?
Numbness Paraesthesia (pins and needles or tingling) Burning sensation Pain
469
What are the motor symptoms of Carpal Tunnel Syndrome?
Weakness of thumb movements Weakness of grip strength Difficulty with fine movements involving the thumb Wasting of the thenar muscles (muscle atrophy)
470
What nerve is affected in Carpal Tunnel Syndrome? Which branch is involved for the sensory symptoms?
MEDIAN Nerve Sensory Sx: Palmer Digital Cutaneous Branch
471
What are the tests to diagnose Carpal Tunnel Syndrome?
Phalen Test Tinel Test
472
What is the Phalen Test?
Put the backs of their hands together in front of them with the wrists bent inwards at 90 degrees. The test is positive when this position triggers the sensory symptoms of carpal tunnel, with numbness and paraesthesia in the median nerve distribution.
473
What is the Tinel Test?
Tapping Median nerve in carpal tunnel causes sensory Sx (Tinels = Tapping)
474
What is the management for Carpal Tunnel Syndrome?
Wrist splints that maintain a neutral position Steroid injections (hydrocortisone) Surgery - decompression (last resort)
475
What are the nerve roots for the Median Nerve?
C6-T1
476
What can lead to compression of the Median Nerve to cause Carpal Tunnel Syndrome?
Swelling of contents within Carpal Tunnel Narrowing of the Carpal Tunnel
477
What is the nerve roots of the radial nerve?
C5-T1
478
What is the classical presentation of a radial nerve palsy?
Wrist drop (with elbow flexed and arm pronated
479
What muscles are innervated by the Radial Nerve?
BEST: Brachioradialis Extensors of forearm Supinator Triceps
480
What muscles are innervated by the Median Nerve?
2LOAF: - 2 Lumbricals - Opponens pollicis - Abductor pollicis brevis - Flexor pollicis brevis
481
What can cause wrist drop?
Damage to the radial nerve Compression of the radial nerve at the humerus
482
What is the nerve roots of the Ulnar Nerve?
C8-T1
483
What is the classical presentation of an ulnar nerve palsy?
Claw hand (4th/5th fingers claw up)
484
What is the treatment of Wrist drop and Claw hand?
Splint Analgesia
485
What are the nerve roots for the common peroneal nerve?
L4-S1 (Branch off the Sciatic nerve)
486
What is the sign of a Sciatic/Common peroneal nerve Palsy?
Foot drop
487
What Drugs can cause peripheral Neuropathy?
amiodarone isoniazid vincristine nitrofurantoin metronidazole
488
What are the main symptoms of peripheral neuropathy?
numbness and tingling in the feet or hands burning, stabbing or shooting pain in affected areas loss of balance and co-ordination muscle weakness, especially in the feet
489
What is Charcot-Marie-Tooth Syndrome?
Inherited sensory and motor peripheral neuropathy disease caused by an autosomal dominant mutation in PUP22 gene on chromosome17
490
What are the genetics of Charcot-Marie-Tooth Syndrome?
Mutation in PUP22 gene Chromosome 17 + multiple others
491
What is the pathophysiology of Charcot-Marie-Tooth Syndrome?
Generally mutations cause dysfunction of the myelin or axons leading to neuropathy Different mutations in different genes have different pathophysiology's.
492
When do symptoms onset in Charcot-Marie-Tooth Syndrome?
Usually before the age of 10. May appear after 40yrs
493
What are the classical features of Charcot-Marie-Tooth Syndrome?
Foot Drop (common peroneal palsy) Distal muscle wasting (stork legs) Hammer Toes (toes always curled up) Pes Cavus (high foot arches) Peripheral sensory loss Reduce tendon reflexes
494
What is the Diagnostic investigation for Charcot-Marie-Tooth Syndrome?
Clinical Dx Nerve biopsy Genetic Testing
495
What is the treatment for Charcot-Marie-Tooth Syndrome?
Supportive Tx: Physiotherapists Orthopaedics Occupational Therapists
496
What is Duchenne Muscular Dystrophy (DMD)?
X-Linked recessive condition caused by a mutation in the Dystrophin Gene
497
Who presents with DMD?
Boys Exclusively: Age of onset is around 3-5 years old
498
Explain the genetics of DMD?
X linked Recessive condition. Therefore mother with 1 faulty gene: Daughters - 50% chance of being carrier Sons - 50% chance of being affected
499
What is the pathophysiology of DMD?
Lack of Dystrophin gene (vital part of muscle fibre) means that the muscles are not protected from being broken down by enzymes Therefore in DMD you get progressive wasting and weakness of muscle as they are broken down. The muscle tissue is then replaced by fibrofatty tissue Most Px in wheelchair by teenage years
500
What cardiovascular condition is associated with DMD?
DCM Dystrophin gene in heart muscle not present which is normally involved in membrane stability. Therefore in DMD there is damage to the cellular mechanisms causing dilation of ventricles due to wasting of the cardiac muscle causing cardiomyopathy
501
What are the symptoms of DMD?
Child struggles to get up from lying down (GOWER'S sign) Skeletal deformities - scoliosis
502
What are the diagnostic tests for DMD?
Prenatal tests and DNA genetic testing
503
What is Gower's Sign?
Children with proximal muscle wasting stand up in a specific way: They get onto their hands and knees, then push their hips up and backwards like the “downward dog” yoga pose. They then shift their weight backwards and transfer their hands to their knees. Whilst keeping their legs mostly straight they walk their hands up their legs to get their upper body erect
504
What is the treatment for DMD?
Purely Supportive: No cure Physiotherapy Occupational Therapy Medical appliances - Wheelchairs Tx of complications - Scoliosis/DCM
505
What is the life expectancy of a child with DMD?
25-35 years
506
What may be used to slow DMD muscular progression?
Oral steroids have been shown to delay progression by 2 years. Creatine Supplements may improve some strength
507
What is Wernicke's Encephalopathy?
Reversible severe cognitive decline due to severe Vitamin B1 (thiamine) deficiency.
508
What is the cause of Wernicke's Encephalopathy?
Alcohol abuse Alcohol massively decreases Thiamine levels leading to deficiency
509
What is the classic triad of Wernicke's Encephalopathy?
Ataxia Confusion Ophthalmoplegia
510
How is Wernicke's Encephalopathy Diagnosed?
Clinically Recognised Macrocytic Anaemia Deranged LFTs
511
What is the treatment of Wernicke's Encephalopathy?
Parenteral PABRNEX (Vit B1) for 5 days. Oral thiamine Prophylactically
512
What is the main complication of Wernicke's Encephalopathy?
Korsakoff Syndrome: Caused when WE left for too long without Tx Leads to Sx with disproportionate memory loss and irreversible damage.
513
What bacteria causes Tetanus?
Clostridium Tetani (Gram +tve Bacillus anaerobe) Inoculation from dirty soil
514
What is the Pathophysiology of Tetanus?
Tetanospasmin Toxin produced. Travels up axons Blocks the release of the inhibitory neurotransmitters GABA and glycine resulting in continuous motor neuron activity → continuous muscle contraction → lockjaw and respiratory paralysis
515
What is the Treatment for Tetanus?
Primary Vaccine (prevention better than cure) Sx treatment: Muscle relaxants Analgesics - paracetamol Metronidazole - remove residual bacteria
516
What is Creutzfeldt-Jakub disease?
Prion disease "Mad cow Disease" Idiopathic misfolded prion proteins deposited in the cerebrum and cerebellum This leads to severe cerebellar Dysfunction. There is NO Tx
517
How does Creutzfeldt-Jakub Disease Present?
Ataxia Poor memory Behavioural changes Muscle weakness Myoclonus Dementia
518
What is the affect of Botulinum toxin?
Blocks acetylcholine (ACh) release leading to flaccid paralysis
519
What is the epidemiology of brain tumours?
10,000+ new cases per year in the UK 55% are malignant 9th most common cancer (3% of all cancers)
520
What are the main Primary Brian tumours?
Gliomas - Tumour of brain intrinsic tissue (subdivided into tissue type; Astrocytoma, Oligodendroglioma, Ependymoma) Meningioma - tumour of brain lining (meninges) Schwannoma (CN tumours)
521
What is the most common Primary brain tumour?
Astrocytoma (90% of Primary brain tumours) 2nd Most common Paediatric cancer
522
What are the common causes of secondary brain tumours?
Metastases from: Non-Small Cell Lung Cancer (NSCLC) Breast Small Cell Lung Cancer (SCLC) Melanoma RCC Gastric Cancer
523
What is the most common cause of a brain tumour?
Secondary brain tumour from a NSCLC
524
What is the treatment for Secondary brain tumours?
Often Palliative Care (due to being mets from high grade tumours) Chemotherapy
525
What is the WHO grading for an astrocytoma (and other brain tumours)? What is the prognosis for each grade?
Graded 1-4 1 = Benign Pilocytic astrocytoma - Good prognosis 2 = Diffuse Astrocytoma - >5 yrs (10 years average) 3 = Anaplastic Astrocytoma - 2-5 yrs 4 = Glioblastoma - <1 yr
526
How are Brain tumours classified into the WHO grade?
Characterised histologically - Cellularity - Mitotic activity - Vascular proliferation - Necrosis
527
What is a Glioma?
A tumour made arising from the Glial cells: Astrocytoma (glioblastoma multiforme is the most common) Oligodendroglioma Ependymoma
528
What are the symptoms of a brain tumour?
Often ASx when small - progress to varied presentations depending on type and location of tumour. Focal neurological Sx as they develop Will often RAISE ICP causing Headaches: Woken by headache Worse in morning Worse Lying down Associated with N+V Exacerbated by coughing, sneezing and drowsiness Papilledema (due to raised ICP) Cushing Triad (Increased PP, Bradycardia, Irregular Breathing) Epileptic Seizures Cancer Sx: Lethargy Malaise Weight Loss
529
What are the red flag signs of a brain tumour?
Headaches: With features of raised ICP (including papilloedema) With focal neurology, check for field defect Other urgent referrals: - New onset focal seizure - Rapidly progressive focal neurology (without headache) - Past history of other cancer
530
What is papilloedema?
Swelling of the optic disc that occurs secondary to a raised ICP. This is often picked up on Fundoscopy
531
What is a Glioblastoma multiforme?
Glioblastoma (GBM), also referred to as a grade IV astrocytoma, is a fast-growing and aggressive brain tumour Often fatal within 1 year of Dx
532
What are the investigations for a brain tumour?
MRI head - locate tumour Biopsy - determine grade Fundoscopy - Papilloedema due to raised ICP NO LP as this is CI in raised ICP
533
What is the management of brain tumours?
Depends on Type, Grade and Site: Tx is non-curative except for Grade I tumours Surgical removal if possible/reduce ICP (dexamethasone to reduce oedema) Chemotherapy/Radiotherapy Before/during/after surgery. (Radiotherapy is mainstay of treatment) Palliative Care
534
What are the differential Diagnoses of a brain tumour?
Aneurysm Abscess Cyst Haemorrhage Idiopathic intracranial hypertension
535
What are Pituitary Tumours?
- Pituitary gland – sits in pituitary fossa (behind nose and below base of brain) - Tumours are almost always benign and usually curable - Excessive effects of tumour - Local effects of tumour – bitemporal hemianopia - Inadequate hormone production by the remaining pituitary gland - Treated with Transsphenoidal surgical resection
536
- What does Cn1 innervate? - What are it's functions? What is its test?
Olfactory - Innervates: olfactory epithelium. - Function: olfaction. - Test each nostril for smell sensation
537
- What does Cn2 innervate? - What are it's functions? What are its tests?
Optic: - Innervates: retina. - Function: vision. pupillary light reflex Visual Acuity Visual Fields
538
- What does Cn3 innervate? - What are it's functions? What are its tests?
Occulomotor: - Innervates: medial, superior and inferior rectus muscles and inferior oblique and levator palpebrae superioris. - Motor function: movement of eyeball. - Parasympathetic function: constriction and accommodation. pupillary light reflex lateral deviation
539
- What does Cn4 innervate? - What are it's functions? What are its tests?
Trochlear: - Innervates: superior oblique. - Functions: movement of eyeball. Elevation of the eye
540
- What does Cn5 innervate? - What are it's functions? What are its tests?
Trigeminal: - Sensory innervation: face, scalp, cornea, nasal and oral cavities, anterior 2/3 of tongue, dura mater. - Motor innervation: muscles of mastication and tensor tympani. - Sensory function: general sensation. - Motor functions: open and close the mouth. Tenses tympanic membrane. Corneal Reflex Open and close mouth
541
- What does Cn6 innervate? - What are it's functions? What are its tests?
Abducens: - Innervates: lateral rectus. - Function: eye movement, abduction. Medial deviation
542
- What does Cn7 innervate? | What are its tests?
Facial: - Special sensory innervation: anterior 2/3 of tongue - taste. - Motor innervation: muscles of facial expression and stapedius. - Parasympathetic innervation: submandibular and sublingual and lacrimal glands. lacrimation Facial Weakness? UMN or LMN Hearing - hyperacusis Corneal Reflex
543
- What does Cn8 innervate? - What are it's functions? What are its tests?
Vestibulocochlear: - Innervation: cochlea and vestibular apparatus. - Functions: hearing and proprioception of head and balance. Cover ear and whisper into the opposite one caloric test
544
- What does Cn9 innervate? | What are its tests?
Glossopharyngeal: - Sensory innervation: posterior 1/3 of tongue, middle ear, pharynx, carotid bodies. - Motor innervation: stylopharyngeus. - Parasympathetic innervation: parotid gland. examined with CNX
545
- What does Cn10 innervate? | What are its tests?
Vagus: - Sensory innervation: pharynx, larynx, oesophagus, external ear, aortic bodies, thoracic and abdominal viscera. - Motor innervation: soft palate, larynx, pharynx. - Parasympathetic innervation: CV, respiratory and GI systems. hoarseness of voice / nasal sound Gag reflex (afferent CNIX and efferent CNX) contraction of the palate and deviation away from lesion
546
- What are the functions of Cn10?
- Sensory functions: general sensation. - Motor functions: speech and swallowing. - Parasympathetic functions: control over CV, respiratory and GI systems.
547
- What are the functions of Cn9?
- Sensory functions: general sensation, taste, chemo/baroreception. - Motor functions: Swallowing (larynx and pharynx are elevated). - Parasympathetic function: salivation.
548
- What are the functions of Cn7?
- Sensory function: taste. - Motor function: facial movement and tension of ossicles. - Parasympathetic function: salivation and lacrimation.
549
- What does Cn11 innervate? - What are it's functions? What are its tests?
Accessory: - Innervation: trapezius and sternocleidomastoid. - Functions: movement of head and shoulders. turn head against resistance shrug shoulders
550
- What does Cn12 innervate? - What are it's functions? What are its tests?
Hypoglossal - Innervation: intrinsic and extrinsic muscles of the tongue. - Function: movement of the tongue. stick tongue out look for signs of deviation. ipsilateral side is paralysed