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Sandra Phase 2a > Neuro > Flashcards

Neuro Flashcards

1
Q

wTypes of strokes:

A

Ischaemic stroke

Haemorrhagic stroke

Can also get a transient ischemic attack

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2
Q

What is a stroke

A

WHO definiton: rapidly developing clinical signs of focal/general disturbance of cerebral function with symptoms lasting 24hours or longer or leading to death, with no apparent cause other than vascular origin

patients with similar symptoms due to: tumours, subdural haemotoma, poisoning, trauma are not considered strokes

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3
Q

Stroke vs TIA

A

TIA: brief episode of neurological dysfunction typically lasting less than 1 hour (up to 24hour) with a vascular cause and with no evience of infarction (cell death) on imaging

Stroke: rapidly developing clinical signs of focal/general disturbance of cerebral function with symptoms lasting 24hours or longer or leading to death, with no apparent cause other than vascular origin

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4
Q

Ischaemic Stroke

A

87% of strokes are ischaemic
occurs due to blockage of blood flow
Ischaemic tissue is weaker and at a bleeding risk -> risk of haemorrhagic transformation

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5
Q

Mechanisms of ischaemic stroke

A
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6
Q

Circle of Willis anatomy

A
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7
Q

Signs and symptoms of ischaemic stroke (Bamford (oxford) classification)

A

Based on clinical findings
Internal carotids: Anterior circulation
Vertebral arteries: Posterior circulatoin

  1. Total Anterior Circulation Syndrome
    Entire anterior circulation of one side - proximal middle cerebral artery often
    All 3 of: 1. Unilateral motor/sensory deficit (2/3 of arm, leg, face)
    2.Higher dysfunction: dyshagia, visuospatial disturbance, reduced consciousness
    3.Homonymous hemianopia
  2. Partial Anterior Circulation Syndrome
    Part of anterior circulation of one side
    2/3 of above symptoms
    OR partial motor/sensory deficit (one limb)
    OR higher dysfunction alone
  3. Posterior Circulation Stroke
    Can also involve cerebellum and brainstem
    cerebellar signs
    cranial nerve and contralateral motor and sensory deficits
    bilateral motor/sensory deficits alone
    isolated homonymous hemianopia
  4. Lacunar Stroke Syndrome
    Subcortical Infarcts <2cm
    Occlusion of penetrating arteries
    1.Pure motor
    2.Pure Sensory
    3.Ataxic Hemiparesis
    4.Dysarthria/clumsy hand syndrome
    5.Mixed Sensorymotor
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8
Q

Diagnosis for ischaemic stroke

A
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9
Q

Treatment for ischaemic stroke

A
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10
Q

Secondary Prevention of Ischaemic Stroke

A
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11
Q

What is a haemorrhagic stroke

A

15-20% are haemorrhagic
result from vessel rupture

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12
Q

Types of haemorrhagic stroke:

A
  1. Intracerebral haemorrhage
    i)Intraparenchymal: bleeding within brain tissue
    ii)intraventricular: bleeding into the ventricles
  2. Subarachnoid haemorrhage

*These intracranial bleeds are considered strokes, others (epidural/subdural) are not considered strokes

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13
Q

Causes of intracerebral haemorrhage

A

hypertension
arteriovenous malformations
cerebral amyloid angiopathy
Vascular tumpurs
Vasculitis

Can also be secondary to an ischaemic Stroke

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14
Q

Causes of subarachnoid haemorrhage

A

85% of spontaneous subarachnoid haemorrhage are due to rupture of an aneurysm
-Anterior communicating artery 35%
-Internal Carotid 30%
-Middle Cerebral artery 22%

15% due to arteriovenous malformation, coagulopathy, intraparenchymal extension

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15
Q

Signs and symptoms of haemorrhagic stroke

A
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16
Q

Diagnosis of haemorrhagic stroke

A
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17
Q

Treatment/management for haemorrhagic stroke

A
  1. Stabilisation - e.g airway
  2. Blood Pressure
    NICE: 1. Presentation within 6h and SBP 150-220mmHg -> reduce to 130-140mmHg and maintain for 7 days
  3. Presentation after 6h or SBP 220mmHg + -> consider reducing to 130-140mmHg and maintain for 7 days
    Exclusions:
    1.Underlying structural cause (AVM, Aneurysm)
    2.Low GCS (Below 6)
    3.Likely to undergo neurosurgery
    4.Poor prognosis

Agents used:
Labetalol
Nimodipine/nicardipine
Enalapril
Hydralazine

  1. Raised intracranial pressure
    Positional change: Bed to 30
    Osmotic agents: Mannitol
    Hyperventilation therapy
  2. Surgical
    Decompressive craniectomy
    Aspiration
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18
Q

Secondary Prevention of Haemorrhagic Stroke

A
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19
Q

What is a TIA (Transient Ischaemic Attack)

A

Brief period of ischaemia due to emboli/stenosis of brain in the carotid artery

Infarction is very unlikely in a TIA

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20
Q

Causes of TIA

A

Modifiable:
Alcohol
Hypertension
Smoking
Hyperlipidaemia
Diabetes Mellitus
Obesity
High Fat diet
Stress

Unmodifiable:
Age
Family History
Male

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21
Q

Pathogenesis

A

Emboli in carotid artery and plaques leads to impaired perfusion of brain tissue

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22
Q

Symptoms of TIA

A

Contralateral hemiparesis
Dysarthria
Vision problems
Gait disturbance
Carotid bruit on physical exam -> due to atherosclerosis of carotid artery

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23
Q

Diagnosis of TIA

A

Carotid ultrasound
CT of head

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24
Q

Treatment of a TIA

A

Aim is to prevent a stroke
-Antiplatelet medication: clopidagrel
-Decrease lipids via statins

Surgery: carotid endarterectomy (surgical removal of plaque and correction of stenosis if stenosis >70%)

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25
Q

Stroke Diagnosis

A
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26
Q

Acute Treatment/Management of Stroke

A
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27
Q

Chronic/Long Term Treatment of Stroke

A
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28
Q

Prevention of Stroke

A
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29
Q

What are stroke syndromes

A

Collections of signs and symptoms resulting from strokes in different regions of the brain/CNS

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30
Q

What does the anterior cerebral artery supply

A

medial & superior frontal and parietal lobes
corpus callosum
basal ganglia

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31
Q

Signs and symptoms of anterior cerebral artery stroke syndrome

A
  1. Contralateral weakness
    Legs > Arm/Face
    Motor homuniculus distribution
  2. Contralateral Sensory deficits
  3. Abulia
    Absence of willpower or the inability to act decisively
  4. Speech Disturbance
    Transcortical motor aphasia: non-fluent, difficulty intiating speech
    Transcortical Mixed aphasia: speaking + comprehension impairment
  5. Urinary Incontinence
    Voluntary bladder control areas affected
  6. Ipsilateral ataxia + contralateral leg weakness
  7. Bilateral ACA involvement
    Bilateral leg weakness
    Frontal disinhibition
    -Primitive reflexes return e.g grasping, suck reflexes
    -Personality changes
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32
Q

What does the middle cerebral artery supply

A

Temporal Lobe
Anterolateral Frontal lobe
Parietal Lobe

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33
Q

Middle Cerebral Artery - Superior division syndrome

A
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34
Q

Middle Cerebral Artery - Inferior Division Syndrome

A
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35
Q

Middle Cerebral Artery - Gerstmann Syndrome

A
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36
Q

Middle Cerebral Artery- Ataxic hemiparesis

A

No facial Involvement/speech disturbance

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37
Q

What does the posterior cerebral artery supply

A

Occipital lobe
Inferior Temporal Lobe
Thalamus
Midbrain

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38
Q

PCA Stroke Syndrome - Alexia without agraphia

A
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39
Q

PCA Stroke Syndrome - Unilateral Occipital Lobe

A
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40
Q

PCA Stroke Syndrome - Anton Syndrome (Cortical Blindness)

A
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41
Q

PCA Stroke Syndrome - Balint Syndrome

A
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42
Q

PCA Stroke Syndrome - Thalamic Pain Syndrome (Dejerine Roussy Syndrome)

A
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43
Q

PCA Stroke Syndrome - Claude Syndrome

A
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44
Q

PCA Stroke Syndrome - Weber Syndrome

A
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45
Q

Basillar/Vertebral Artery Stroke Syndrome

A
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46
Q

Types of Intracranial Haemorrhage

A

Extra-Axial Haemorrhage: Bleeding that occurs within the skull but outside the brain tissue
Epidural
Subdural
Subarachnoid

Intra Axial Haemorrhage (Inside Brain tissue)
Intracerebral
Intraventricular

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47
Q

What is an epidural haemorrhage?

A

Bleeding between the skull and the dura mater
Source of blood is often arterial (Middle meningeal artery)

Causes:
Skull fractures (70-95%). Head trauma includes: motor vehicle accidnet, fault, assault

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48
Q

Clinical Manifestations of an epidural haemorrhage

A

Altered consciouscness
Headache
Vomiting
Confusion/seizures
Aphagia

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49
Q

What is a subdural haemorrhage

A

Bleeding between the dura mater and subarachoid membrane

Source of blood often tearing of the bridging veins

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50
Q

Clinical Manifestations of a subdural haemorrhage

A

Coma (50%)
Lucid interval -> Progressive neuro decline -> Coma

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51
Q

What is a subarachnoid haemorrhage

A

Haemorrhage within arachnoid space
Source of blood from rupturing of aneurysm (cerebral artery)

Causes:
Rupture of sacular aneurysm -> subarachnoid haemorrhage

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52
Q

Clinical Mainfestations of subarachnoid haemorrhage

A

Sudden severe headache
Loss of consciousness/Seizure
Nausea/Vomiting
Meningismus

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53
Q

Types of intracerebral haemorrhage

A

Lobar haemorrhage
Thalamic haemorrhage
Pontine hameorrhage
Cerebellar haemorrhage

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54
Q

Intracerebral haemorrhage

A

Second most common cause of stroke

Aetiology:
Hypertension
Embolism
Brain tumour
Bleeding Disorder
Drugs

Clinical Manifestations
Neurological signs and symptoms (Depending on area)
Headache
Nausea/Vomiting
Decreased loss of consciousness

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55
Q

Intraventricular haemorrhage

A

Bleeding confined to the ventricular system of the brain

Most often occurs as a secondary phenomenon when intracerebral haemorrhage ruptures or when subarachnoid haemorrhage extends to the ventricles

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56
Q

Diagnosis of intracerebral haemorrhage

A

CT scan
MRI
Angiography

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57
Q

Treatment for intracerebral haemorrhage

A

Drugs
-for hypertension
-to relieve intracranial pressure

Surgery
-Craniotomy: part of skull removed to drain blood and relieve pressure
-Stereotactic aspiration: aspirate off blood and relieve pressure

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58
Q

Pathophisiology of intracerebral haemorrhage

A
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59
Q

Diagnosis of subarachnoid haemorrhage

A
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60
Q

Treatment of subarachnoid haemorrhage

A
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61
Q

Diagnosis of epidural haemorrhage

A
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62
Q

Treatment for epidural haemorrhage

A
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63
Q

Diagnosis for a subdural haemorrhage

A
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64
Q

Treatment for a subdural haemorrhage

A
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65
Q

What is multiple sclerosis?

A

Chronic and progressive autoimmune demyelinating disease of the nerve cells in the brain, spinal cord characterised by various neurological disorders
Cell-mediated (Type IV) hypersensitivity reaction

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66
Q

Pathophisiology of MS

A

Type IV hypersensitivity
1.T cell crosses blood brain barrier. Becomes activated by myelin
2.T cell changes blood brain barrier, expressing more receptors for immune cells to cross blood brain barrier
3. Cytokines (IL-1, IL-6, TNF - alpha, INF- gamma) released by T cells dilates blood vessels (allowing more cells to get in) and directly damages oligodendrocytes
4. Attracts B cells which produce antibodies that mark myelin sheath proteins, And macrophages which use those antibody markers to engulf and destroy oligodendrocytes.
5. Without oligodendrocytes, no myelin covers the neurons leaving sclera
6. Attacks happen in bouts

Early on: remyelination occurs
Overtime: Irreversible

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67
Q

Causes of MS

A
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68
Q

Types of MS

A
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69
Q

Charcot’s neurological triad

A
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70
Q

Symptoms of MS

A

Vary, depends on location of plaques
Affects 20-40 years old
Worsen over weeks;linger for months
Charcot’s neurological triad

Also (see pic)

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71
Q

Diagnosis of MS

A
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72
Q

Treatment for RRMS

A
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73
Q

Treatment for Progressive MS

A
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74
Q

What is Guillain-Barre Syndrome

A

Autoimmine demyelinating disorder that leads to progressive paralysis

Most common cause of acute flaccid, neuromuscular paralysis worldwide

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75
Q

Causes of Guillain-Barre Syndrome

A
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76
Q

Pathophysiology of Guillain-Barre Syndrome

A
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77
Q

Symptoms of Guillain-Barre Syndrome

A
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78
Q

Guillain-Barre Syndrome diagnosis

A
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79
Q

Treatment of Guillain-Barre Syndrome

A
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80
Q

What is Parkinson’s Disease

A

Neurodegenerative condition resulting from loss of dopaminergic neurons in the brain, characterised by associated motor symptoms

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81
Q

Part of brain involved in regulating motor signalling

A

Basal Ganglia

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82
Q

Direct vs Indirect pathway of basal ganglia

A

Direct facilitates movement
Indirect terminates movement

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83
Q

Pathophysiology of Parkinson’s Disease

A

Thought that the degeberation of neurons in substantia nigra pars compacta is due to the accumulation of Alpha’s Nuclein (protein involved in regulation of the synaptic vesicles and release of neurotransmitters)

Close Link to Lewys Body dementia

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84
Q

Signs and symptoms of Parkinson’s Disease

A

Appear when 50% of neurons have been lost
1.Bradykinesia
2.Rigidity (muscle stiffening): Cog wheel rigidity, Lead Pipe rigidity
3.Hypomimia - Expressionless Face
4.Tremors (Pill Rolling Tremor) - Mostly resting
5.Gait Disturbance - Shuffling gait. Also at an increased risk of falls

= Collectively these symtpoms are known as Parkinsonism (80% of Parkinsin’s Disease). Others include
-Drug induced
-Multi-system atrophy
-Progressive Supranuclear Palsy
-Normal Pressure Hydrocephalus

Other symptoms include:
6. Autonomic disturbance: Hypersalivation, constipation/incontinence
7. Cognitive Impairment

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85
Q

Causes of Parkinson’s Disease

A

Most cases are idiopathic

1.Genetics:
-2x risk in 1st degree relatives
-10-15% of cases are familial: Autosomal Dominant, Autosomal recessive

  1. Environmental
    -Rural living
    -Exposure to industrial chemicals
    -Infections: Encephalitis
  2. Age- mean age 60
    -5-15% before 40
    -1% of people over 60
  3. Males : Females (1.5:1)
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86
Q

Diagnosis of Parkinson’s Disease

A

Clinical Diagnosis

Movement Disorder Society Parkinson’s Disease Criteria:
1.Bradykinesia + Resting Tremor/Rigidity
+
2. 2 Supportive Criteria
+
3. No exclusion or red flag criteria

Dat Scan: Radioactive Isotope + SPECT scan

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87
Q

Treatment for Parkinson’s Disease

A
  1. Medication
  2. Deep Brain stimulation:
    -Pulse generator placed under skin
    -Electrodes placed in vicinity of basal ganglia
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88
Q

Parkinsons Disease: On/Off phenomenon

A

Initially medication may treat symptoms well however as time goes on there is less of an effect and the on/off phenomenon inevitably appears with the use of levodopa. Overtime the window for controlled symtpoms known as the on phase gets tighter. While off is a state of rigidity and uncontrolled symptoms. The switch from on to off and vice versa can happen quickly. This kinesias are involuntary movements that are a side effect that can occur when patients flip between on and off known as diphasic dyskinesia. It can also occur following levadopa medication giving peak dopamine levels known as peak dose dyskinesia.

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89
Q

What is Huntington’s Disease

A

Huntington disease, or HD, is a rare neurodegenerative disease that involves a repeated sequence of DNA that causes an abnormal protein to form, leading to abnormal movements and cognitive problems.

Autosomal Dominant genetic disorder

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90
Q

Cause of HD

A

Mutation in a single gene called huntingtin. This is a dominant mutation. Thus if 1 parent has the disease, their child has a 50% chance of developing it too.

The huntingtin gene contains a DNA sequence that consists of nucleotides (CAG) in repitition - known as trinucleotide repeat. When the gene is mutated an excess no of repeats can occur and a mutated form of huntington protein is created.
The higher the noof repeats the greater the risk of disease, and all people with 36 or more repeats in the huntingtin gene will develop Huntington’s disease. Mutated Huntingtin proteins ahve a tendency to group together, forming clusters within neuros that are not easily removed by brai enzymes. Accumulation in the brain is associated with increased neurodegeneration.

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91
Q

Symptoms of HD

A
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92
Q

Regions affected by Huntington’s

A
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93
Q

Diagnosis of Huntington’s Disease

A

MRI
EEG

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94
Q

Treatment for HD

A
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95
Q

What is dementia?

A

Progressive neurodegenerative disease characterised by cognitive decline that causes impairment in daily functioning

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96
Q

Types of dementia

A

1.Alzheimer’s Disease
2.Vascular dementia
3.Dementia with Lewy Bodies
4.Frontotemporal dementia

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97
Q

Signs and symptoms of dementia

A

Symptoms get progressively worse over time

Cognitive Decline >=1 of:
1.Memory
2.Executive Function
3.Language
4.Attention
5.Visuospatial function

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98
Q

Alzheimer’s disease

A

70% of dementia

Caused due to the accumulation of insoluble proteins in the brain:
beta amyloid plaques: extracellular
hyperphosphorylated Tau protein (normally involved in microtubules): intracellular neurofibrillary tangles

Beta amyloid may be found in non-dementia brains
-Increased quantity in Alzheimer’s
-Mostly hippocampus , parietal, temporal lobes

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99
Q

Symptoms of Alzheimer’s disease

A

1.Short term memory loss
2.Difficulty finding words
3.Disorientation
4.Poor insight

100
Q

Vascular Dementia

A

Involves reduced blood flow to neurons giving ischaemia and cell death

1.Multi Infarct Dementia
Series of small strokes that together cause symptoms

  1. Subcortical dementia
    Small penetrating arteries affected (small vessel disease)
  2. Stroke related dementia
    30% of ischaemic strokes

Function decreases in a step-wise manner

101
Q

Risk Factors for Vascular dementia

A

1.Smoking
2.Diabetes
3.AF
4.Dyslipidaemia
5.Hypertension
6.Age

Risk doubles every 5 years

102
Q

Risk Factors for Vascular dementia

A

1.Smoking Diabetes

103
Q

Prominent symptoms of Vascular dementia

A

Impairment in :
Planning
Organising
Judgement occur early on

104
Q

Dementia with Lewy Bodies

A

10%

Lewy Bodies: Spherical, intracellular deposits formed from alpha synuclein + ubiquitin

Primary abnormality in Parkinson’s Disease dementia

105
Q

Symtpoms of dementia with Lewy Bodies

A

Core symptoms
1. Flucuating cognition
2. Visual hallucinations (2/3)
3. Parkinsonian Features: Bradykinesia, rigidity, falls, autonomic dysregulation(orthostatic hypotension, incontinence/constipation)

Suggestive symptoms
1.REM sleep disturbances
2.Sensitivity to antipyschotics

106
Q

Frontotemporal dementia

A

Second most common dementia in under 65s: mean age of onset 53

Involved proteins:
1.TDP 43 (DNA binding protein)
2.Tau protein (microtubule protein)

Types:
1.Behavioural variant (BvFTD) Pick’s disease
Most common
Personality/behavioural changes early
-Disinhibition/social withdrawal
Pick Bodies: Spherical intracellular collections of tau fibrils

  1. Semantic Variant
    Difficulty finding correct words
    impaired comprehension
    Fluent Aphasia

3.Non fluent variant
Progressively more hesitant speech

=2 + 3 are primary progressive aphasia

107
Q

Risk Factors for dementia

A
  1. Age is the largest risk factor
    -Age 65 = 2%
    -Age 85 = 40%
  2. Genetics:
    -10-30% increased risk in 1st degree relative
    -Early Onset dementia (<65years): Trisomy 21,
    5% of alzheimer’s overall (and majority of early onset) has autosomal dominant inheritance with near complete penetrance
    Early genes: Late genes:
  3. APP Ch21 1. Apolipoprotein E: E4 variant (1 allele = 50%)(2 allele = 90%) 2. Presenilin 1 Ch14
  4. Presenilin 2 Ch 1
  5. Gender: F>M
  6. Cognitive Reserve
    Social isolation
    Left education early
    Low job complexity
  7. Vascular Risk Factors
108
Q

Diagnosis of dementia

A

Post mortem brain biopsy traditionally only mode of confirmation
-Rarely done on living people
-PET scan can demonstrate histological features of Alzheimer’s

1.Clinical History + Physical Exam

2.Mental State Examination: MMSE/MOCA

3.Lab investigations:
Blood typically normal
Vitamin B12/Folate
Thyroid Function Tests
Electrolyte Panels
Infection (e.g Lyme’s disease + neurosyphilis)

  1. CT head
    Exclusion of chronic intracranial bleed or normal pressure hydrocephalus
    Cerebral atrophy
  2. Genetic Testing
109
Q

What is the most common cause of death in dementia

A

Pneumonia

110
Q

Treatment for dementia

A

No cure currently

1 year mortality 30-40%. 5 year mortality 65%

1.Medication
Cholinesterase inhibitors: donepezil, galantamine, rivastigmine)
NMDA antagonists: memantine
= slow cognitive decline but effect on survival unclear

  1. Risk Reduction (Especially vascular)
  2. Behavioural + Environmental support
    Maintain familiarity
    Monitor personal comfort
    Attention redirection

4.Mental Health Support
5.Aerobic exercise

111
Q

Types of CNS infections:

A

Meningitis (bacterial, viral and fungal)

Encephalitis

112
Q

What is meningitis

A

Inflammation of the leptomeninges (arachnoid and pia maters)

113
Q

What is meningoencephalitis

A

Meningitis : Inflammation of the leptomeninges
+
Encephalitis : Inflammation of the brain

114
Q

Pathophisiology of meningitis

A

Inflammation triggered by:
1.Autoimmune disease: Lupus
2.Adverse reaction to medication: Intrathecal therapy (injected directly into CSF)
3.Infection (most common): Neisseria meningitidis, Herpes simplex

2 routes an infection takes to reach CSF and leptomeninges
1.Direct spread (Pathogen gets inside skull/spinal column and penetrates the meninges and eventually CSF):
Through overlying skin
Up through nose
Anatomical defect: congenital (spina bifida). acquired (skull fracture)
2. Haemotogenous spread
Through binding to surface receptors/areas of damage/vulnerable spots

Pathogen recognised by CSF and produces more white blood cell. 1ul Greater than 5 WBC -> meningitis

115
Q

Meningitis: Common causative organisms table

A
116
Q

Symptoms of meningitis

A

Stiif and Painful Neck
Fever
Altered Mental Status
Headache
Photophobia & Phonophobia
Malaise & Fatigue
Nausea/Vomiting
Anorexia
Skin Rash
Cold Extremities
Papilledema: Swelling of optic nerve due to increased ICP
Seizures
Cranial Nerve Palsies

117
Q

Diagnosis for meningitis

A

Kernig’s sign
Brudzinski’s sign
Lumbar puncture (needle between L3 & L4 takes CSF): Measure pressure, analyse WBC, protein & glucose
PCR: Look for HIV, Enterovirus, HSV, TB
Western Blot: Borrelia burgdorferi
Thin Blood Smear: Malaria

118
Q

Treatment for meningitis

A
119
Q

What is encephalitis?

A

Condition involving inflammation of the brain parenchyma
May be due to a variety of causes

120
Q

Epidemiology & Risk Factors for developing encephalitis

A
121
Q

Causes of encephalitis

A
122
Q

Pathogenesis of encephalitis

A
123
Q

Clinical Features of encephalitis

A

Other Features:
Meningitis signs and symptoms
Nuchal rigidity (“Stiff neck”)
Brudzinski’s sign
Kernig’s sign

124
Q

Diagnosis of encephalitis

A
125
Q

Treatment of encephalitis

A
126
Q

Primary vs Secondary type headache

A
127
Q

Tension type headache

A

Most ubiquitus headache and is the most common reason why OTC analgesics are purchased
Location: Bilateral
Character: Pressure or toghtness which waxes and wanes
Duration: Variable
Associated symptoms: None

128
Q

Migraine headache

A

A disorder of recurrent attack
Location: Unilateral (70%)
Character:
gradual onset, crescendo pattern, moderate-severe intensity
Duration: 4-72 hours
Associated symptoms: nausea, vomiting, photophobia, phonophobia, aura

129
Q

Cluster headache

A

Form of trigeminal autonomic cephalgia
0.1% of population
“Suicide headache” - excruciating
Unilateral -Eye/Temple
<4hr duration
Sweating, tearing, hypermia, ptosis, rhinorrhea, restlessness
Cyclical/Consistent timing
Precipitated by alcohol
More common in men and smokers

Episodic: episodes present on 7-365 days of the year with at least 1 month complete remission
Chronic: pain ongoing beyond 1 year, less than 1 month complete remission

Treatment :
Acute:
1. Oxygen therapy
2. Triptans

Prevention:
1. Verapamil (CCB)
2. Lithium
3. Topiramate
4. Deep Brain/Occipital Nerve stimulation

130
Q

What is trigeminal neuralgia

A

Neurological condition involving recurrent episodes of facial pain

131
Q

Pathophysiology of trigeminal neuralgia

A
132
Q

Signs and symptoms of trigeminal neuralgia

A
133
Q

Diagnosis of trigeminal neuralgia

A

Clinical diagnosis
MRI to rule out secondary causes (lesions)

134
Q

Treatment for trigeminal neuralgia

A

1st line therapies:
Carbamazepine
Oxcarbazepine

135
Q

What are seizures

A

Transient occurence of signs and symptoms due to abnormally excessive or synchronous neuronal activity within the brain

136
Q

Classification of seizures

A

1st: where the seizure originated in the brain
Generalised: Involve both hemispheres of the brain
Focal: Originate from an area on one hemisphere
*If seizures begin on one hemisphere and then involve both sides, they are known as focal to bilateral seizures

2nd: whether or not patient keeps their awareness during the seizure
Generalised seizures are automatically considered to affect awareness, only applies to focal seizures
Focal Aware = Simple
Focal Unaware = Complex

3rd: Motor/Non-motor involvement during the seizure
Generalised seizures may feature stiffening and jerking
Focal Seizures can have movements twitching, jerking and stiffening + automatic movements like licking lips or rubbing hands
Focal seizures: one group of muscles may be affected but abnormal movement can spread to other muscle groups . Due to abnormal neuronal activity of brain also moving to a diff area - JACKSONIAN MARCH.
Generalised non-motor seizures are known as absent seizures where individuals will rpimarily have changes in awareness and stay
Focal non-motor seizures typically have other symptoms that happen first (aura) e.g changes in emotion/sexperiences/thinking

137
Q

Types of generalised seizures

A
138
Q

What is status epilepticus

A

> 5 mins seizure duration
Medical emergency
Benzodiazepine, phenytoin, phenobarbital

139
Q

What is the postictal phase

A

Following a seizure there is a postictal phase
Lasts min-hours
Confusion
Tiredness
Headache
Speech difficulty
10% pyschosis
Amnesia

140
Q

Causes of Seizures. Provoked or Unprovoked?
VITAMINS

A
141
Q

Diagnosis of seizures

A
142
Q

Management of seizures

A
  1. Follow up - specialist clinic
    Antiepileptic drugs: valproate, lamotrigine, levetiracetam
143
Q

Differential diagnosis for seizures

A
144
Q

What is an upper motor neuron

A

Neuron located within brain/brainstem
Axon travels down spinal cord
Innervates alpha & gamma motor neurons in ventral horn

145
Q

What is a lower motor neuron

A

Alpha & Gamma motor neurons located in the ventral horn of the spinal cord
Axon travels to periphery to innervate muscle

146
Q

UMN vs LMN lesions

A
147
Q

Signs of upper vs lower motor neuron lesions

A
148
Q

What is myastenia gravis

A

Acquired autoimmune condition involving neuromuscular blockade and subsequent muscle weakness
It is a type II hypersensitivity reaction
Most common neuromuscular junction disorder affecting skeletal muscles

149
Q

Classic presentation of myasthenia gravis

A

Fluctuating muscle weakness and fatigue of heavilt used muscle groups
-Worsens with activity and improves with rest
-Weakness worse in the afternoon hours
-Weakness involves muscles of the eyes, extremities and throat

Extraocular Muscle Weakness
-Ptosis, Diplopia (often none in morning): Unilater or bilateral
-Often intial finding
-Most common symptom

Ocular MG -> Generalised MG

Continuing see pic

150
Q

Pathophysiology of myasthenia gravis

A

Autoantibodies produced against acetylcholine receptors & other muscle components

151
Q

Myasthentic crisis

A
152
Q

Myasthenia gravis : exacerbating factors

A
153
Q

Types of myasthenia gravis

A
154
Q

Differential Diagnosis of Myasthenia Gravis

A

Lamber-Eaton Syndrome (Paraneoplastic)
Guillain Barre Syndrome
Motor Neuron Disease

155
Q

Course of Myasthenia Gravis

A
156
Q

Investigations for Myasthenia Gravis

A
157
Q

Treatment for Myasthenia Gravis

A
158
Q

What is motor neurone disease

A

Cluster of major degenerative diseases
Characterised by selective loss of neurons in motor cortex, cranial nerve nuclei and anterior horn cells
Upper and lower motor neurones are affected, but there’s NO sensory loss or sphincter disturbance – distinguishes from MS and polyneuropathies
Never affects eye movements – distinguishes from myasthenia
Relentless and unexplained destruction of upper motor neurones and anterior horn cells
Most will die in 3yrs from respiratory failure due to bulbar palsy and pneumonia

159
Q

Causes of motor neurone disease

A

Most are sporadic with no family history
Rare familial cases
Mutations in the free radical scavenging enzyme copper/zinc superoxide dismutase (SOD-1)
Suggests that oxidative stress and free radicals play a role in destruction of motor neurones

160
Q

Clinical presentation (symptoms and signs) of motor neurone disease

A

4 clinical patterns:
ALS/amyotrophic lateral sclerosis – 50%
Loss of motor neurons in motor cortex AND anterior horn of cord
Weakness + UMN signs e.g. upgoing planters
+ LMN wasting/fasciculation
Worse prognosis if – bulbar onset, older, reduced FVC
Split hand sign- thumb’s side of the hand seems to separate from the rest owing to excessive wasting around it

Progressive bulbar palsy – 10%
Only affects cranial nerves IX-XII
LMN lesion of the tongue and muscles of talking and swallowing –
Flaccid, fasciculating tongue
Jaw jerk is normal or absent
Speech is quiet, hoarse or nasal

Progressive muscular atrophy – 10%
Anterior horn cell lesion only
No UMN signs
Affects distal muscle groups before proximal

Primary lateral sclerosis
Loss of Betz cells in motor cortex
Mainly UMN signs
Marked spastic leg weakness and pseudobulbar palsy
No cognitive decline

Suspect MND in
>40yrs
Stumbling spastic gait, foot-drop ± proximal myopathy
Weak grip and shoulder abduction

UMN signs – spasticity, brisk reflexes, upgoing plantars

LMN signs – wasting, fasciculation of tongue, abdomen, back, thigh

161
Q

Diagnostic tests and results for motor neurone disease

A

Brain/spinal cord MRI excludes structural causes
Lumbar puncture excludes inflammatory ones

162
Q

Treatment for motor neurone disease

A

Antiglutamatergic drugs – riluzole
Drooling – propantehline, amitriptyline
Dysphagia – blend food, NG tube
Spasticity – baclofen, diazepam
Joint pains and distress – follow analgesic ladder
Respiratory failure – non-invasive ventilation at home may allow palliation

163
Q

What is a spinal cord compression

A

Metastatic spinal cord compression (MSCC) is an oncological emergency that describes when tumours (usually having spread from another part of the body) grow in the spinal column and compress the spinal cord.

L1-L2 anything below is cauda equina syndrome

164
Q

Causes of spinal cord compression

A

Spinal metastases
-Lung
-breast
-myeloma
-lymphoma
-prostate

165
Q

Signs and symtpoms of spinal cord compression

A
166
Q

Diagnosis of spinal cord compression

A

MRI

167
Q

Management of spinal cord compression

A
168
Q

What is cauda equina syndrome

A

Cauda equina syndrome is a condition caused by damage to the bundle of peripheral nerves protruding from the bottom of the spinal cord, called the cauda equina.

169
Q

Causes of cauda equina syndrome

A
170
Q

Symptoms of cauda equina syndrome

A
171
Q

Diagnosis of cauda equina syndrome

A
172
Q

Treatment of cauda equina syndrome

A
173
Q

Spinal cord lesions summary

A
174
Q

What is syncope

A

Reversible loos of consciousness due to inadequate blood flow to the brain

-Fast onset
-Short duration
-Spontaneous recovery

175
Q

Causes of syncope

A
176
Q

Diagnosis of syncope

A
177
Q

Causes of syncope (PASS OUT)

A
178
Q

symptoms of syncope

A

Blacking out.
Feeling lightheaded.
Falling for no reason.
Feeling dizzy.
Feeling drowsy or groggy.
Fainting, especially after eating or exercising.
Feeling unsteady or weak when standing.
Changes in vision, such as seeing spots or having tunnel vision.
Headaches.

179
Q

Treatment for syncope

A

Medicines for syncope include:
Midodrine.
Fludrocortisone

180
Q

Limb neuropathies..

A
  • Carpal tunnel syndrome
  • ‘Wrist drop’
  • ‘Claw hand’
  • ‘Foot drop’
181
Q

What is carpal tunnel syndrome

A

Cindition involving impingement (or entrapment) of the median nerve in the wrist
Most common entrapment neuropathy

182
Q

Pathophysiology of carpal tunnel syndrome

A

Median nerve becomes compressed in the carpal tunnel due nto bone growth and/or soft tissue proliferation

183
Q

Risk factors for carpal tunnel syndrome

A
184
Q

Clinical Features of Carpal Tunnel Syndrome

A
185
Q

Diagnosis of Carpal Tunnel Syndrome

A
186
Q

Treatment for carpal tunnel synrome

A
187
Q

What is a foot drop? (Peroneal Nerve Injury)

A

The patient is unable to lift the front of the foot up due to weakness or paralysis of the tibialisi anterior muscle which lifts the foot up

188
Q

Signs of a foot drop

A

When the patient with foot drop walks, the foot slaps down onto the floor

Steppage gait means that the patient slaps his foot down onto the floor because the foot drops, and his gait will show that he is raising the thigh up in an exagerrated fashion while walking

189
Q

Causes of a foot drop

A

Usually results from an injury to the common peroneal nerve. This nerve is susceptible to injury at any point of its course

Conditions causing foot drop:
1.L4-L5 disc herniation: Herniated disc compressing the L5 nerve root may cause foot drop

2.Lumbrosacral plexus injury can occur from a pelvic fracture with displacement of the sacriliac joint

3.Hip/Knee dislocation

4.Neglected compartment syndrome

Systemic causes: diabetes, ischaemia, inflammatory conditions

190
Q

Causes of a foot drop

A

Usually results from an injury to the common peroneal nerve. This nerve is susceptible to injury at any point of its course

Conditions causing foot drop:
1.L4-L5 disc herniation: Herniated disc compressing the L5 nerve root may cause foot drop

2.Lumbrosacral plexus injury can occur from a pelvic fracture with displacement of the sacriliac joint

3.Hip/Knee dislocation

4.Neglected compartment syndrome

Systemic causes: diabetes, ischaemia, inflammatory conditions

191
Q

Treatment of foot drop

A

Non operative treatment:
Observation
Therapy
Stretching
Range of motion of the ankle
AFO bracing

Surgery:
Nerve repair/grafting if there is laceration of the nerve
If the injury is chronic, you will do a posterior tibial tendon transfer to the lateral cuniform, in addition to achilles tendon lengthening

Split posterior tibial tendon transfer

192
Q

What is wrist drop

A

characterisitic deformity of a radial nerve lesion

The wrist remians in the palamr flexion due to weakness of the dorsiflexions. It is seen in radial nerve palsy

193
Q

Causes of wrist drop

A

Radial nerve = big

Trauma
-Shoulder dislocation
-Fractures (Humerus, supracondylar, monteggia)

Compression
-Saturday Night Palsy
-Crutch Palsy

194
Q

Treatment for wrist drop

A

Tendon transfer operation

195
Q

What is claw hand

A

Ulnar nerve palsy
Claw hand is a condition that causes curved or bent fingers

196
Q

Causes of claw hand

A

Causes may include:

Congenital abnormality
Genetic diseases, such as from Charcot-Marie-Tooth disease
Nerve damage in the arm
Scarring after a severe burn of the hand or forearm
Rare infections, such as leprosy

197
Q

Diagnosis of claw hand

A

Medical History
Physical Examination
Electromyography

198
Q

Treatment for claw hand

A

Physical therapy
Surgery

199
Q

What causes amaurosis fugax

A

Atherosclerotic emboli in the eye

Heart disease, especially irregular heartbeat
Alcohol abuse
Cocaine use
Diabetes
Family history of stroke
High blood pressure
High cholesterol
Increasing age
Smoking (people who smoke one pack a day double their risk for a stroke)
Amaurosis fugax can also occur because of other disorders such as:

200
Q

When can amaurosis fugax occur

A

Amaurosis fugax can also occur because of other disorders such as:

Other eye problems, such as inflammation of the optic nerve (optic neuritis)
Blood vessel disease called polyarteritis nodosa
Migraine headaches
Brain tumor
Head injury
Multiple sclerosis (MS), inflammation of the nerves due to the body’s immune cells attacking the nervous system
Systemic lupus erythematosus, an autoimmune disease in which the body’s immune cells attack healthy tissue throughout the body

201
Q

What is Lambert-Eaton Syndrome

A

Rare Autoimmune Neuromuscular junction disorder -> presynaptic neurons

This is due to a decreased Ach release and therefore reduced contraction

Improves temporarily after repeated use

202
Q

Majority of Lambert-Eaton Syndrome cases are associated with

A

Small Cell Lung Cancer

Also associated with:
Hashimoto’s thyroiditis
Diabetes Mellitus type 1

203
Q

Causes of Lambert-Eaton Syndrome

A

Autoimmune response against voltage-gated Ca2+ chnnels
Affects somatic and parasympathetic nervous system
Type II hypersensitivity reaction: antibody production against its own protein

Antibodies bind and block most Ca2+ channels: Low Ca2+ with neuron -> no Ach release -> no muscle contraction

With repeated stimulation -> enough Ca2+ gets through -> Ach release -> muscle contraction

204
Q

Signs and symptoms of Lambert-Eaton Syndrome

A

Symmetrical weakness of proximal muscles
-Shoulders, hips and thighs
-Difficulty climbing stairs and standig up

Reduced reflexes

Warming-up phenomenon: weakness is relieved temporarily after repeated use

Advanced stages: weakness in the respiratory muscles -> respiratory failure

Most have autonomic symptoms: dry mouth, constipation, blurred vision, urinary problems, fainting

205
Q

Diagnosis of Lambert Eaton Syndrome

A
206
Q

Treatment of Lambert Eaton Syndrome

A
207
Q

What is brown Sequard Syndrome

A

Condition that results from damage (resection) to one half of the spinal cord on either side

This hemisection causes damage of the spinal cord tracts

This syndrome results in weakness or paralysis (hemiparaplegia) on one side of the body and a loss of sensation (hemianesthesia) on the opposite side

Damages:
Descending Corticospinal tracts
Ascending dorsal column tracts
Spinothalamic tracts

208
Q

How does sensory stimuli reach brain

A

A sensory stimuli passes through three neurons

The lateral branch of the 1st order neuron carries info to the dorsal root

The second order neuron crosses over to the opposite side of the spinal cord

Third order neuron located in the ventral posterior region of the thalamus to the sensory cortex of the brain

209
Q

What causes Brown Sequard Syndrome

A
210
Q

Symptoms of Brown Sequard Syndrome

A
211
Q

Diagnosis of Brwon Sequard Syndrome

A

MRI

212
Q

Treatment of Brown Sequard Syndrome

A
213
Q

What is Charcot-Marie-Tooth syndrome

A

Group of hereditary, progressive neurlogical disorders of the PNS, impaired sensory/motor function

Inherited

Worsen overtime

214
Q

Pathophysiology of Charcot-Marie-Tooth Syndrome

A

Defective proteins in myelin sheath or axon -> signals fail to reach target tissues: sensory & motor

215
Q

Types of Charcot-Marie-Tooth Syndrome

A

CMT1: Autosomal dominant
Mutations in PMP22 & MPZ: Encode proteins part of myelin sheath (made by schwann cells)
Slows down electrical impulses

CMT2: Autosomal dominant
Mutations in MFN2: Encodes Mitofusin-2 (expressed in neuronal mitochondria)
When defective: mitochondrial function (-> neuronal death)-> disrupted

in both CMT1 & CMT2, motor neurons are affected, muscles begin to atrophy (“use it or lose it”). When sensory nerves are affected the feet and toes are first affected

216
Q

Symptoms of Charcot-Marie-Tooth Syndrome

A
217
Q

Diagnosis of Charcot-Marie-Tooth

A
218
Q

Treatment of Charcot-Marie-Tooth

A
219
Q

Duchenne muscular Dystrophy (D mnemonic)

A
220
Q

Diagnosis of duchenne muscular dystrophy

A

presence of risk factors
imbalance of lower limb strength
lower extremity musculotendinous contractures
delayed motor milestones

221
Q

Diagnostic investigations of duchenne muscular dystrophy

A
222
Q

Treatment for muscular dystrophies

A

stage 1: ambulatory
1ST LINE –
corticosteroids

stage 2: non-ambulant
1ST LINE –
supportive therapies to maintain activities of daily living

stage 3: ventilator-supported
1ST LINE –
inspiratory and expiratory respiratory muscle assistance

223
Q

What is depression

A

A mental state of low mood

224
Q

Diagnostic and Statistic Manual of Mental Disorders (DSM V)

A
225
Q

Causes/Risk Factors of depression

A

Multifactorial
1. Genetics
High concordance rates in twins
Family History

  1. Environmental
    Stressful life events
    Childhood abuse
    Substance abuse/medical conditions

Diasthesis-Stress model:
See pic

226
Q

Pathophysiology of depression

A

Not entirely understood

  1. Monoamine theory: lack of monoamine neurotransmitters (serotonin, dopamine, norepinephrine)
    Decrease in serotonin is not equal to depression in healthy individuals
    Anti-depressants restore levels quickly, but take weeks to improve clinical symptoms
  2. Hypothalamic-Pituitary Axis Disturbance
    Increase Cortisol, decrease dexamethasone suppression
    Link to growth + thyroid hormones
  3. Immune system
    Excessive cytokine release
    Improvement of symptoms with NSAIDs
    Close link between asthma and depression
227
Q

Epidemiology of depression

A
  1. Lifetime risk ~ 12%
  2. Female : Male 2:1
    Different pyschosocial pressures
    Hormonal Diff
  3. Mean onset ~ 40 years
    Becoming increasingly common in younger ages
228
Q

Diagnosis of depression

A
229
Q

Treatment for depression

A

Combinations more effective

1.Lifestyle

2.Pyschotherapy *Favoured in U18s: CBT, interpersonal therapy

3.Medication:
SSRI: Setraline, citalopram, fluoxetine
SNRI: Duloxetine, venlafaxine
Atypical: mitrazapine
TCA (amitriptyline)
MAOI (selegiline)
Vit D
COX-2 inhibitors (Celecoxib)

  1. Electroconvulsive therapy
    Electrically Induced Seizure
    50% effective in treatment resistant MDD. 50% relapse in 12 months
230
Q

Primary vs Secondary brain tumours

A

Primary: Tumour in the brain that arose from associated tissue

Secondary: Tumour in the brain that metastasised there from elsewhere

231
Q

Types of primary brain tumours

A

Glioma
Meningioma
Pituitary adenoma

232
Q

Clinical Presentation of primary brain tumours

A

Progressive focal neurological deficit: Symptoms depend on location (frontal lobe -> personality change etc). Speed of deterioration is proportional to growth of tumour Raised intracranial perssure: Headaches (worse on cough/leaning forward), vomiting and papilloedema. Epilepsy: Focal or generalised General cancer symptoms: Weight loss, malaise, anaemia etc

False localising signs: Raised ICP or the presence of a tumour can cause healthy structures to affect adjacent ones. E.g., Downward displacement of temporal lobe -> III or VI CN palsy

233
Q

Pathophysiology of primary brain tumours

A

Progressive focal neurological deficit: Mass effect of the tumour and oedema -> impact functionality of site associated with tumour. Can destroy tissue -> rapid deterioration Raised ICP: As tumour grows -> downward displacement of the brain -> pressure on the brainstem (drowsiness) -> respiratory depression -> coma -> death. False localising signs possible (see left) Epilepsy: Tumour creates unusual electrical impulses -> seizures

234
Q

Causes of primary brain tumours

A

Derived from the skull itself, or adjacent structures. 95% of primary tumours are Gliomas or Meningiomas (others include neurofibromas and lymphomas)

235
Q

Causes of secondary brain tumours

A

Metastases from: Bronchus, Breast, Kidney, Thyroid, Stomach, Prostate

236
Q

Epidemiology of Primary brain tumour

A

About 10% of all neoplasms

237
Q

Diagnosis of primary brain tumour

A

CT and MRI. Positron Emission Tomography to find occult metastasis

238
Q

Treatment of primary brain tumours

A

Surgery: Exploration, removal or biopsy (meningiomas can be fully removed without incident)

Radiotherapy: Gliomas and radiosensitive metastases

Medical: Cerebral oedema can be reduced with corticosteroids. Epilepsy treated with anticonvulsants.

239
Q

What is peripheral neuropathies

A

Neuropathy of the peripheral nerves

240
Q

Types of peripheral neuropathies

A

3 types: autonomic, motor and sensory

241
Q

Clinical Presentation of peripheral neuropathies

A

Can be asymptomatic. Diabetes: Long history of paresthesia (glove stocking), pain, weakness and wasting, autonomic symptoms; incontinence, sexual dysfunction). Usually present as foot ulcers (constant damage due to paresthesia)

242
Q

Pathophysiology of peipheral neuropathies

A

Diabetes: Hyperglycaemia damages 3 cell types; retinal endothelium, mesangial cells in glomeruli and schwann cells in perpheral nerves (these cell types cannot regulate their glucose well, so constant hyperglycaemia causes excessive oxidation -> damage)

243
Q

Aetiology of peripheral neuropathies

A

Acute: Guillain barre Chonic: Diabetes, alcohol

244
Q

Diagnosis of peripheral neuropathies

A

Nerve conduction studies. FBC. Diabetes: As in DM

245
Q

Treatment for peripheral neuropathies

A

Diabetic control. Amitriptyline for neuropathic pain.

Sandra Phase 2a (17 decks)

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