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CNS > Clinical Medicine > Flashcards

Clinical Medicine Flashcards

1-30 LMNL and disorders of peripheral nerves 31-48 Spinal Cord Disorders 49-66 Disorders of Neuromuscular Junctions 67-82 Ischemic and Hemorrhagic Strokes 83-100 UMNL and Localization of Cortical Lesions 101-122 Cerebellar and Balance Disorders 123-162 Increased Intracranial Pressure 163-208 Movement Disorders 209-220 Sleep Disorders 221-263 Infections in CNS 267-320 Headache 321-335 Delirium 336-355 Neurological Disorders affecting Vision

1
Q

What are some causes of UMNL?

A

Stroke
MS

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2
Q

What are some causes of LMNL?

A

Polyneuropathy
GBS
Early UMNL

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3
Q

What are the signs of LMNL?

A

Flaccidity
Decreased DTR
Present atrophy
Fasciculation
Weakness pattern: [Distal > Proximal, Flexors = Extensors]

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4
Q

What are the signs of UMNL?

A

Spasticity
Increased DTR
Clonus
Absent Superficial reflexes
Positive Babinski
Positive Hoffman
Disuse atrophy
Weakness pattern: [UL: Extensors > Flexors, LL: Flexors > Extensors]

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5
Q

What are the 4 phases of spinal shock and its duration?

A

Areflexia [0-1 day]
Initial reflex return [1-3 days]
Hyperreflexia [1-4 weeks]
Hyperreflexia, spasticity [1-12 months]

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6
Q

What is the cause of spinal muscular atrophy?

A

Genetic - AR

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7
Q

Describe the clinical presentation of Spinal Muscular atrophy

A

Progressive muscle weakness and atrophy

LMNL

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8
Q

Treatment of Spinal Muscular Atrophy?

A

ASO- antisense oligonucleotide

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9
Q

What is ALS?

A

Neurodegenerative disease affecting motor neurons in cerebral cortex, brainstem and anterior horn of SC

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10
Q

Describe the presentation of ALS?

A

Progressive weakness that spreads one limb to the other and eventually patients die due to respiratory failure
Mixed UMNL and LMNL

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11
Q

Prognosis of ALS?

A

Fatal in 3-5 years

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12
Q

What is an example of sensory neuronopathy?

A

Herpes zoster [الحزام الناري]

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13
Q

Describe presentation of plexopathy?

A

Weakness and numbness depending on parts of plexus affected

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14
Q

What are some causes of plexopathy?

A

DM
Focal mas - Pacoast

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15
Q

What is a hereditary cause of peripheral neuropathy?

A

Charcoat Marie Tooth disease

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16
Q

What is mononeuropathy?

A

One peripheral nerve is affected

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17
Q

What are some examples of mononeuropathy?

A

CN7 palsy
Carpal tunnel syndrome

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18
Q

What causes carpal tunnel syndrome?

A

Median nerve entrapped in flexor retinaculum

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19
Q

What are the symptoms of carpal tunnel syndrome?

A

Numbness in lateral 3 ½ digits +/- weakness

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20
Q

What are the clinical exams for carpal tunnel syndrome?

A

Tinel sign
Phalen sign

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21
Q

How is carpal tunnel syndrome diagnosed?

A

Clinical diagnosis
Nerve conduction study

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22
Q

What is used to treat Carpal tunnel syndrome?

A

Wrist splint/NSAIDs
Steroid
Surgery

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23
Q

What is mononeuropathy multiplex?

A

Several peripheral nerves affected simultaneously or sequentially

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24
Q

What are some causes of mononeuropathy multiplex?

A

Vasculitis of vasa nervorum
Sarcoidosis
DM

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25
Q

What is polyneuropathy?

A

Generalized symmetric and length dependent [Longest fibers affected first]

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26
Q

What is the commonest cause of polyneuropathy?

A

DM

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27
Q

How is polyneuropathy diagnosed?

A

Clinical diagnosis
Nerve biopsy [if necessary]
Nerve conduction study [to confirm diagnoses and classify it]

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28
Q

What are the types of polyneuropathy?

A

Demyelinating
axonal

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29
Q

What are the causes of axonal neuropathy?

A

Metabolic /endocrine [DM]
Hereditary
Drugs
Vasculitis
Vitamin toxicity
Alcohol

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30
Q

What are the causes of demyelinating neuropathy?

A

GBS
Hereditary
Arsenic toxicity
Lymphoma

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31
Q

Describe the presentation of Anterior Spinal Artery Syndrome

A

Areflexia + flaccid paralysis at lesion [anterior horn destruction]
Anhidrosis + loss of vasomotor tone
Loss of bladder + bowel control but with preservation of reflex emptying
Paralysis of respiration in cervical segments
Bilateral horn syndrome

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32
Q

What structures are affected in Anterior Spinal artery Syndrome?

A

Anterior ⅔ of SC, with sparing of posterior columns and horns

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33
Q

In what order are the structures affected in Syringomyelia? What is the correlating presentation?

A

Anterior horn cells → LMNL patterns
Corticospinal tract → caudal UMNL signs
2nd order Spinothalamic fibers as they decussate anterior to anterior ventral commissure

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34
Q

Describe the clinical presentation of Syringomyelia

A

Cape sensory deficit / sacral sparing

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35
Q

What are the causes of Syringomyelia?

A

Hemorrhage
Trauma
Tumor of SC
Chiari I malformation

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36
Q

Describe the presentation of Combined system degeneration?

A

Loss of motor function below lesion
Loss of position sense below lesion
Loss of vibratory sensation below lesion

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37
Q

What structures are affected in combined system degeneration?

A

Lateral corticospinal tract
Dorsal Columns

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38
Q

What structures are affected by Vit. B12 deficiency?

A

Diffuse involvement of dorsal columns and lateral corticospinal tracts
Optic nerve, cerebellum, peripheral nerves and cerebral hemisphere

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39
Q

What are the causes of Combined system degeneration?

A

Vitamin B12 deficiency
Hypocupremia myelopathy

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40
Q

What structures are affected in Tabetic syndrome?

A

Large posterior fibers of dorsal roots that later form the posterior column

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41
Q

What are the causes of Tabetic Syndrome?

A

Tertiary neurosyphilis
DM

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42
Q

Describe the presentation of Complete transection

A

Decreased in respiration if above C5
Spasticity below lesion [UMNL]
Decreased voluntary bowel and bladder control

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43
Q

What are the causes of complete transection?

A

Transverse myelitis [post-infectious or demyelinative]
Corticospinal tract
Dorsal column

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44
Q

What are the structures affected in Complete transection?

A

Anterolateral spinothalamic tract
Dorsal columns

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45
Q

Describe the clinical presentation of hemisection syndrome

A

Ipsilateral sensory loss below the lesion
Contralateral motor loss [LMNL]

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46
Q

What structures are affected in hemisection syndrome?

A

Anterolateral spinothalamic tracts
Dorsal column

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47
Q

What is another name for Brown-sequard syndrome?

A

Hemisection syndrome

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48
Q

What are the causes of hemisection syndrome?

A

Trauma
Compression
MS

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49
Q

What is the cause of Myasthenia Gravis?

A

Antibodies against N1 Ach Receptors [Post-synaptic]

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50
Q

What is the cause of LEMS?

A

Antibodies against VGCC [Pre-synaptic]

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51
Q

What is the cause of Botulism?

A

C. Botulism neurotoxin [Pre-synaptic]

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52
Q

What is the cause of Organophosphate Exposure?

A

Irreversible inhibition of AchE → ↑↑Ach stimulation [Synaptic]

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53
Q

Describe the onsets of Botulism, MG, and LEMS

A

Botulism: Rapid onset
MG + LEMS: Progressive onset

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54
Q

What conditions are associated with MG?

A

Autoimmune diseases [Hyperthyroidism]
Lymphoma [10%]

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55
Q

What conditions are associated with LEMS?

A

Small cell cancer

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56
Q

Describe the clinical presentation of MG

A

Fatigability with repetitive contraction with diurnal variation
Ptosis & Diplopia [in 2/3]
Descending weakness
Facial Weakness
Snarl Smile
Dysarthria & Dysphagia
Proximal Muscle Weakness
Respiratory Muscle weakness [MG Crisis]
Normal sensation & Reflexes

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57
Q

Describe the clinical presentation of LEMS

A

Ascending weakness
Slow progressive leg weakness & fatigue
Dry Mouth
Constipation
Post-Exercise Facilitation
Eye & Bulbar symptoms [in 30%]
Absent Deep Tendon Reflex

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58
Q

Describe the clinical presentation of Botulism

A

Dilated Pupils
Dry mouth
Constipation
Descending weakness

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59
Q

Describe the clinical presentation of Organophosphate Exposure

A

Proximal Muscle Weakness
Respiratory Muscle weakness
Confusion, Anxiety
Coma
Diarrhea
Vomiting
Sweating

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60
Q

Diagnostic tests for Botulism?

A

Incremental response
Toxin Isolation

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61
Q

Diagnostic Tests for LME?

A

Incremental response w/↑ frequency stimulation
CT chest for SCLC
Antibodies against VGCC in 95% of patients

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62
Q

Diagnostic Tests for MG?

A

Decremental response w/↓ frequency stimulation
CT chest for Thymoma
AchR-Ab in 85% of patients
MuSK-Ab in 50% of patients who test -ve for AchR-Ab
Tensilon Test [IV Tensilon causes temporary and rapid improvement of symptoms]

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63
Q

Treatment of OE

A

Atropine
Pralidoxime

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64
Q

Treatment of Botulism

A

Penicillin G
Botulinum Toxin
Toxin Removal [Gastric Lavage + Wound cleaning]

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65
Q

Treatment of LEMS

A

3,4-DAP [potassium channel blocker]

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66
Q

Treatment of MG

A

Pyridostigimine [temporary symptomatic treatment]
Glucocorticoids → Steroid-spacing mechanisms
Thymectomy
IV Ig
PE

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67
Q

What is a stroke?

A

Sudden focal neurological deficit caused by interruption of blood flow to a specific region of the brain

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68
Q

What are the two types of strokes?

A

Hemorrhagic
Ischaemic

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69
Q

What are the common types of stroke?

A

Ischaemic [85%]
Intracerebral hemorrhage [15%]
SAH [5%]

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70
Q

What is the most common cause of emboli in ischemic stroke?

A

Atrial Fibrillation

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71
Q

What is a Transient Ischemic attack?

A

Focal deficit that resolves completely and spontaneously within 24 hours
[60% have evidence or brain infarction]

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72
Q

What are the risk factors for stroke?

A

HTN
Smoker
DM
Dyslipidemia
Previous history of TIAs
Heart disease
Hypercoagulopathy
Sickle cell/ Increased RBCs
Obesity
Carotid Bruit
Afib
Snoring
Cocaine

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73
Q

What is the most common artery implicated in strokes?

A

Middle Cerebral Artery

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74
Q

Describe the presentation of MCA occlusion?

A

Contralateral face
Aphasia [if on left]
Contralateral sensory loss
Cortical sensory loss [non-dominant hemispheres]
Contralateral visual field defect
Gaze deviation ipsilateral to lesion

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75
Q

Describe the presentation of Internal Cerebral artery occlusion

A

Ipsilateral retinal ischemia
Sensorimotor dysfunction similar to MCA

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76
Q

Describe the presentation of ACA occlusion

A

Contralateral leg weakness
Contralateral leg sensory loss
Apraxia
Abulia

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77
Q

Describe the presentation of PCA occlusion

A

Contralateral homonymous hemianopia
Visual agnosia
Cognitive dysfunction

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78
Q

Management of Suspected Stroke cases

A

CT angiogram
EEG
Neurological screening assessments
IV with normal saline

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79
Q

When should CT scan be done?

A

Within 25 minutes of arrival

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80
Q

Management of Hemorrhagic Strokes?

A

Mannitol to lower ICP
Nimodipine for SAH

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81
Q

Management of Ischemic strokes

A

Consider fibrinolytic [tPA] therapy or Aspirin

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82
Q

Secondary prevention of TIAs?

A

Evaluate for embolism or carotid stenosis
Aspirin / Clopidogrel

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83
Q

What structures are affected in capsular hemiplegia?

A

Corticospinal tracts
Corticobulbar tracts

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84
Q

Occlusion of which artery may lead to capsular hemiplegia?

A

MCA

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85
Q

What is a characteristic finding of capsular hemiplegia?

A

Ipsilateral facial nerve palsy, with sparing of the upper half

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86
Q

Signs of UMNL in the Internal Capsule?

A

Contralateral hemiplegia
Hemisensory loss
UMN signs

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87
Q

Signs of UMNL in Midbrain?

A

Crossed hemiplegia
Ipsilateral oculomotor palsy
Contralateral hemiplegia

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88
Q

Signs of UMNL in Pons?

A

Contralateral hemiplegia
Ipsilateral CN 6, CN 7 palsy

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89
Q

Signs of UMNL in Medulla?

A

Ipsilateral CN 9, 10, 11, 12 palsy
Contralateral hemiplegia

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90
Q

Signs of UMNL in the cervical area?

A

Ipsilateral hemiparesis

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91
Q

What determines the dominant hemisphere?

A

Localization of speech and mathematical ability

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92
Q

When is cerebral dominance established?

A

1st few years of life

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93
Q

What would produce primitive reflexes?

A

Bilateral lesion of frontal cortex

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94
Q

What are the functions of the Frontal lobe?

A

Planning ahead
Monitoring
Sustained attention
Goal orientated behavior
Working memory
Problem solving

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95
Q

What are the functions of the parietal lobe?

A

Receives and processes sensory information
Transmits info to other parts and coordinates
Visual attention
Spatial reasoning

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96
Q

Tests for Parietal lobe?

A

Sterogeneis test
Point discrimination test
Graphesthesia test

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97
Q

What are the functions of the temporal lobe?

A

Hearing
Compression of Language
Memory retrieval and formation

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98
Q

What would a lesion in Wenicke’s area produce?

A

Affects language comprehension, response would also be gibberish

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99
Q

Lesion of which structure would produce homonymous hemianopia?

A

Optic tracts

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100
Q

Lesion of which structure would produce homonymous hemianopia with macular sparing?

A

Cerebral cortex

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101
Q

What is the function of the anterior cerebellar lobe?

A

Regulates muscle tone

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102
Q

What is the function of the posterior cerebellar lobe?

A

Coordination of voluntary motor activity

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103
Q

What is the function of the flocculonodular lobe?

A

Maintenance of posture and balance

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104
Q

What are the characteristics of cerebellar disease?

A

Hypotonia [rag-doll appearance and inebriated]
Disequilibrium
Dyssynergia
Dysmetria [past-pointing]
Ataxia
Dysarthria
Intention tremor
Dysdiadochokinesia
Nystagmus

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105
Q

What is dysdiadochokinesia?

A

Inability to perform rapid alternating movements

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106
Q

How can we check for rebound?

A

Flex forearm at elbow against resistance, then suddenly release, positive if it hits chest or face

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107
Q

Describe decomposition of movements?

A

Breakdown smooth muscle act into jerky parts
Rebound

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108
Q

Cause of Anterior Vermis Syndrome

A

Alcohol abuse [commonly]

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109
Q

Presentation of Anterior Vermis Syndrome

A

Gait, trunk and leg ataxia

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110
Q

Presentation of Posterior Vermis Syndrome

A

Gait ataxia

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111
Q

What Structure is affected in Posterior Vermis Syndrome?

A

Flocculonodular lobe

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112
Q

What are the common causes of Posterior Vermis Syndrome?

A

Brain tumors in children, ex:
Medulloblastoma
Ependymoma

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113
Q

What are the causes of Cerebellar hemispheric syndrome?

A

Brain Tumor
Brain abscess

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114
Q

Presentation of Cerebellar Hemispheric Syndrome?

A

Ipsilateral Leg/Arm, Truncal and Gait ataxia

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115
Q

Cause of Anterior Lobe Syndrome?

A

Malnutrition associated with chronic alcoholism

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116
Q

Manifestation of Anterior Lobe Syndrome?

A

Ataxic gait
Gait instability
Loss of coordination
Fails heel-shin test
Dysarthria

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117
Q

Cause of Posterior Lobe Syndrome?

A

Strokes
Tumor
Trauma
Degenerative disease

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118
Q

Manifestation of Posterior Lobe Syndrome

A

Decreased muscle tone
Intention tremor
Loss of coordination of voluntary movements
Explosive speech
Dysmetria
Dysdiadochokinesia

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119
Q

Manifestation of Floculondular Lobe Syndrome?

A

Truncal Ataxia- Paraxial muscles

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120
Q

What produces appendicular ataxia?

A

Lesion of cerebellar hemispheres

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121
Q

Causes of Intention Tremors?

A

MS
Midbrain infarction

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122
Q

Ataxia mimicers

A

Hydrocephalus → damages frontopontine pathways

Lesion of prefrontal cortex

Pons/Cerebellar peduncles → cerebellar input or output

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123
Q

What does Monro-Kellie rule state?

A

An increase in one element [Blood, CSF, Brain Tissue] must occur at the expense of others, which will increase ICP

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124
Q

What is the normal ICP in adults?

A

8 - 18 mmHg
15 - 22 cmH20

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125
Q

What is the normal ICP in children?

A

10 - 20 cmH20

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126
Q

What is the leading cause of Increased ICP in kuwait?

A

Idiopathic intracranial HTN, associated with obesity

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127
Q

What is the formula for CPP?

A

CPP = MAP - ICP

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128
Q

What is the normal CPP?

A

80-100 mmHg

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129
Q

What is the formula for MAP?

A

MAP = DP+ ⅓(SP-DP)

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130
Q

What is the most reliable indicator of increased ICP?

A

Decreased LOC

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131
Q

What is the earliest sign of ↑ICP? Late sign?

A

Early sign: Decreased LOC
Late sign: Fixed and dilated pupil

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132
Q

What is cushing’s triad?

A

Bradycardia
Change in breathing pattern
↑BP

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133
Q

What causes cushing’s triad?

A

Ischemia or pressure on brainstem

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134
Q

Describe decorticate posturing

A

Flexion of UL and extension of LL
[Plantar flexed
Internally rotated
Flexed arm, elbow and hands
Adducted shoulders]

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135
Q

Describe decerebrate posturing

A

Extension of UL + LL
[Plantar flexed
Extended elbow
Pronated forearm
Flexed hand]

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136
Q

What is a sign of ↑ICP in infants?

A

Bulging fontanelle

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137
Q

What are signs of ↑ ICP?

A

Headache
Vomiting
Abnormal posturing
Papilledema
Poor pupillary response to light

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138
Q

What respiratory changes are associated with diffuse cortical lesions?

A

Cheyne-stokes respiration

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139
Q

What is Cheyne-stoke respiration?

A

Apnea alternating with hyperventilation

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140
Q

What respiratory changes are associated with Midbrain lesion?

A

Central Neurogenic Hyperventilation

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141
Q

What is Central Neurogenic Hyperventilation?

A

Sustained regular and rapid, deep breathing

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142
Q

What respiratory changes are associated with pons lesion?

A

Apneustic breathing

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143
Q

What is Apneustic breathing?

A

Prolonged pause at end of inspiration

144
Q

What respiratory changes are associated with medullary lesion?

A

Ataxic breathing

145
Q

What is ataxic breathing?

A

Rapid and shallow breathing

146
Q

Describe pupillary changes associated with brainstem lesion

A

Midbrain: Mid-sized pupils
Pons: Pin-point pupils

147
Q

What are the types of brain edema?

A

Vasogenic
Cytotoxic
Interstitial

148
Q

What is the most common type of brain edema?

A

Vasogenic

149
Q

What is Vasogenic Edema?

A

Increased permeability of brain capillary endothelial cells , follows white matter distribution

150
Q

Cause of Vasogenic Edema?

A

Tumor
Abscess
Hemorrhage
Infarction
Contusions

151
Q

What is Cytotoxic Edema?

A

ATP failures, increasing cell size, follows gray matter distribution

152
Q

Cause of Cytotoxic Edema?

A

Hypoxic-ischemic injury
Osmolar injury
Toxins
Secondary injury following head trauma

153
Q

What is interstitial edema?

A

Increase of water content of periventricular matter due obstruction of CSF flow

154
Q

Herniation Syndrome due to increased ICP?

A

Transtentorial herniation
Subfalcine herniation
Central herniation
Upward transtentorial herniation
Tonsillar herniation

155
Q

What structures are compressed in transtentorial herniation?

A

Ipsilateral Oculomotor
PCA
Rarely- Contralateral Oculomotor nerve + Cerebral peduncle

156
Q

What is transtentorial herniation?

A

Medial temporal lobe squeezed under tent

157
Q

What is Subfalcine herniation?

A

Cingulate gyrus pushed under falx cerebri

158
Q

What structures are compressed in subfalcine herniation?

A

ACA [→ infarction of paramedian cortex]

159
Q

Treatment of Increased ICP

A

Removal of causative
Hyperventilation [→ hypocapnia → vasoconstriction]
Removal of CSF
Fluid restriction
IV mannitol
Steroids

160
Q

What is Upward Transtentorial herniation?

A

Infratentorial mass compresses brain stem → upward movement of cerebellum

161
Q

Presentation of Central Herniation:

A

Hernites both temporal lobes → damage to midbrain:
Decerebrate posturing
Pupils fixed in mid positions
→ Loss of brainstem reflexes/cessation of respirations/brain dead

162
Q

What are the indications for corticosteroids as treatment for ↑ICP?

A

Brain tumor
Abscesses

163
Q

What are the classes of hyperkinetic disorders?

A

Tics
Myoclonus
Ballismus
Dystonia
Chorea
Atherosis
Tremor

164
Q

What are the classes of hypokinetic disorders?

A

Parkinsonism

165
Q

What is most common major movement disorders?

A

Parkinson’s disease

166
Q

What is the typical age of onset of parkinsons?

A

50-60 yrs

167
Q

What are the cardinal features of PD?

A

Bradykinesia
Rigidity
Instability [postural]
Tremor [Resting]

168
Q

What are the symptoms of Parkinson’s?

A

Stooped posture
Masked facial expression
Forward tilt of trunk
Rigidity
Flexed elbows and wrists
Slightly flexed hips and knees
Shuffling, short stepped gait
Trembling of extremities

169
Q

What is the most disabling symptom of PD?

A

Bradykinesia

170
Q

What is the earliest sign of PD?

A

Resting tremor

171
Q

Define resting tremor

A

Tremor that presents at rest and improves when a motor task is performed

172
Q

Describe resting tremors in PD?

A

Begins unilaterally as “pill-rolling” tremor in hands
Earliest sign of PD, present in 70% of patients

173
Q

What sign is indicative of advanced stage of PD?

A

Postural instability and gait disturbances

174
Q

Describe the postural instability seen in PD?

A

Flexion of neck and trunk

175
Q

Describe gait disturbances seen in PD?

A

Low gait with short stride length
Inability to turn quickly
Reduced arm swing

176
Q

What rigidity is seen in PD patients?

A

Lead pipe [sustained] rigidity
Cogwheel [intermittent] rigidity
[lead pipe + tremor]

Seen in 90% of patients

177
Q

What signs are common in parkinsonisms?

A

Rigidity
Bradykinesia

178
Q

How do you diagnose PD?

A

History & clinical examination

2 out of 4 cardinal features

Laboratory tests and imaging

To exclude secondary parkinsonism

Diagnosis supported by response to Dopaminergic drugs

179
Q

What is the treatment of PD?

A

Dopamine replacement
Amantadine
MAO-B inhibitors
DBS

180
Q

Classification of Parkinsonism?

A

Primary
Secondary
Atypical

181
Q

What are the causes of atypical parkinsonian syndromes?

A

Corticobasal degeneration [CBD]

Progressive Supranuclear palsy [PSP]

Multiple System Atrophy [MSA]

182
Q

What are tics?

A

Sudden, repeated, brief movement or sounds, which can be voluntarily suppressed

183
Q

What is the clinical criteria for Tourette Syndrome?

A

≥2 motor
≥ 1 vocal
> 1 year

184
Q

What is coprolalia?

A

Profanities

185
Q

What is echolalia?

A

Repeat what others say

186
Q

What is palilalia?

A

Repeats own words

187
Q

What is dystonia?

A

Sustained involuntary muscular contraction → fixed posture / repetitive twisting movements

188
Q

Divisions of Dystonia?

A

Focal
Generalized
Task specific

189
Q

What is torticollis?

A

Dystonia of neck

190
Q

What are the task specific dystonias?

A

Writer’s cramp
Musician dystonia
Throwing a ball

191
Q

What is sensory trick?

A

Purposeful movement that suppresses dystonia

192
Q

What medications may cause dystonia?

A

Dopamine receptor blockers

193
Q

Define myoclonus

A

Brief shock-like jerks

194
Q

What is an example of negative myoclonus?

A

Asterixis

195
Q

What can myoclonus indicate?

A

Lesion in cortex, subcortex, brainstem, spinal and peripheral nerves

196
Q

Define tremors

A

Rhythmic oscillation of a body part by alternating contraction of antagonist muscles

197
Q

What structures are affected by tremors?

A

Hands
Head
Jaw
Voice
Tongue
LL

198
Q

What are the causes of resting tremors?

A

PD

199
Q

How are tremors classified?

A

Resting tremor
Postural tremor
Action tremor

200
Q

What is the commonest movement disorder?

A

Essential tremor

201
Q

How are essential tremors diagnosed?

A

Spiral test

202
Q

What are the treatment options of Essential tremor?

A

Medications [propranolol]
Deep brain stimulation

203
Q

What is chorea?

A

Irregular, involuntary, non-rhythmic and unsustained movements that flow from one side to another

204
Q

What are the classic examples of chorea?

A

HD
Sydenham’s chorea

205
Q

What are two hereditary causes of chorea? Its pattern of inheritance?

A

HD - [dominant]
Wilson’s disease [recessive]

206
Q

What is ballismus?

A

Large amplitude choreic movements of proximal limbs

207
Q

What is the commonest cause of hemiballismus?

A

Stroke

208
Q

What is athetosis?

A

Slow continuous stream of sinuous, writhing movements [typically of hands]

209
Q

What is the most common sleep disorder?

A

Insomnia

210
Q

Define Acute Insomnia?

A

Few days - 3 months, usually results of stressful events

211
Q

Define Chronic Insomnia?

A

> 3 months

212
Q

What is Restless leg syndrome?

A

Urge to move legs, accompanied/caused by uncomfortable sensations in legs, worsening during periods of rest and is relieved by movement

213
Q

What are the supportive features of Restless leg syndrome?

A

Dopaminergic responsiveness
Positive family history
Presence of periodic limb movements in sleep/wakefulness

214
Q

Clinical manifestations of Narcolepsy

A

Narcoleptic sleep attacks
Distrubed night sleep
Cataplexy
Hallucination/Automatic behaviors
Sleep paralysis

215
Q

Comorbid conditions associated with Narcolepsy?

A

Periodic limb movements
Sleep Apnea
Rem sleep behavior disorder
Eating disorders
Increased BMI
DM

216
Q

What is narcolepsy?

A

Irresistible desire to fall asleep at inappropriate times

217
Q

Pathophysiology of narcolepsy?

A

Depletion of hypocretin neurons in lateral and prefrontal region of hypothalamus

218
Q

Diagnostic test of narcolepsy?

A

Decreased hypocretin 1 in CSF
HLA-DQB1-0602 in Ch.6

219
Q

Presentation of Narcolepsy?

A

Agr 15-30, runs in family 1-2 of first degree relatives

220
Q

What are parasomnias?

A

Abnormal movements that occur in sleeper during arousals from sleep, with preserved sleep architecture

221
Q

In general, how do infectious microorganisms cause disease in the CNS?

A

Direct invasion of neuronal tissue

Production of neurotoxin

Immune response incited by pathogen

222
Q

Infection by which microorganisms present acutely?

A

Viral and Bacterial [mostly]

223
Q

Infection by which microorganisms present sub-acutely/chronically?

A

Mycobacterium
[+Neurosyphilis]
Fungal
Parasitic
Spirochetal

224
Q

What signs and symptoms indicate meningitis?

A

Fever
Neck Rigidity
Headache
Vomiting

225
Q

What signs and symptoms indicate encephalitis?

A

Seizures
Altered sensorium

226
Q

What are the causes of infectious encephalitis?

A

Viral [Commonest]
Bacterial
Fungal
Autoimmune
Para/Post-Infectious

227
Q

What are the clinical features of focal encephalitis?

A

Changes in :
Consciousness
Alert
Behavior
Personality
Focal seizures

228
Q

What are the clinical features of generalized encephalitis?

A

Generalized seizures
Altered sensorium
Confusion
Coma
Irritability
Confusion
Disorientation
Prodrome [Fever, headache, Body aches, and N &V]

229
Q

What is the most serious cause of encephalitis and its pathogenesis?

A

HSV 1 , Through the olfactory nerves

230
Q

Describe the clinical presentation of Generalized encephalitis?

A

Acute onset
Generalized seizures
Neurological deficit [possible]

231
Q

Describe the clinical presentation of Focal encephalitis

A

Subacute onesie
Focal seizures
Neurological deficit

232
Q

What are the clinical features of Generalized encephalitis?

A

Headache
Fever
Vomiting
Agitation
Restlessness
Altered sensorium
Unconsciousness

233
Q

What are the clinical features of Focal encephalitis?

A

Conscious with behavioral or personality changes

234
Q

What are the investigative tests for encephalitis?

A

Routine lab tests
Blood Cultures
CSF exam
PCR
Serology by detection of antibodies in CSF
CT/MRI
EEG

235
Q

What does CSF of an encephalitic patient show?

A

CSF analysis
↑ protein
Normal glucose
Lymphocytic pleocytosis

236
Q

What viral causes of encephalitis are treatable?

A

VCZ
HSV
CMV

237
Q

What is the empirical treatment for encephalitis?

A

Acyclovir

238
Q

When is acyclovir withdrawn in encephalitis patients?

A

If HSV+ VCZ excluded

239
Q

What is the symptomatic management of encephalitis?

A

Mannitol for cerebral edema
Anticonvulsants for seizures
Steroids

240
Q

What are the complications of Encephalitis?

A

Brain edema
Personality changes
Memory problems
SIADH
Intellectual disorders
Lack of muscle coordination
Paralysis
Epilepsy
Hearing or vision defects
Speech impairment
Coma
Death

241
Q

What is the common etiology of Generalized encephalitis?

A

Viral, short-lived

242
Q

What is the common etiology of Focal encephalitis?

A

HSV
Autoimmune

243
Q

What is the cause of HSE?

A

Reactivation of virus lying dormant in trigeminal ganglion

244
Q

What investigations are used to diagnose HSE?

A

CSF analysis
HSV PCR
CT: uni/bilateral temporal lobe lesion
EEG
Repeat all investigation after 4 days if initially negative

245
Q

Prognosis of HSE

A

Mortality > 70% with severe long term neurological sequelae

W/treatment ~30% but with severe disabilities

246
Q

Describe the clinical presentation of viral meningitis

A

Acute onset and symptoms may follow a preceding flu-like symptoms
Fever and severe headache
Meningeal irritation, N &V, rashes
Less common: Diarrhea, myalgia, cough

247
Q

What are the most common causes of viral meningitis?

A

Enterovirus
HSV 1
HSV2

248
Q

CSF analysis of Viral meningitis

A

Normal/ ↑ protein
Normal glucose
Lymphocytic pleocytosis
Normal or slightly elevated opening pressure

249
Q

When is IV acyclovir indicated in viral meningitis?

A

HSV 1/HSV 2
VCZ

250
Q

What is the prognosis of viral meningitis?

A

Self limited infections, with adults making a complete recovery within 7-10 days

251
Q

Sequelae of Viral meningitis in children?

A

Seizures
Hydrocephalus
Sensorineural hearing loss
Cognitive/behavioral abnormalities

252
Q

Describe the presentation of acute bacterial meningitis in elderly patients

A

Possibly atypical with no signs of meningeal irritation, just non-specific confusion

253
Q

What investigations are used to diagnose bacterial meningitis?

A

CSF exam [gold standard]
CT- possible sulcal effacement
MRI-
T2- hyperintensity in sulci
T1- enhancement of leptomeninges within sulci
DWI- diffusion restriction in sulci

254
Q

What does CSF examination in bacterial meningitis patient reveal?

A

↑ protein
↓↓ glucose
Pleomorphic pleocytosis

255
Q

What is the empirical treatment of acute bacterial meningitis?

A

Vancomycin
Ceftriaxone / Cefotaxime
Dexamethasone

256
Q

Prognosis of bacterial TB?

A

Mortality /Morbidity 18-40%

257
Q

Who has a poor prognosis in bacterial meningitis?

A

Extreme ages
Immunocompromised
Late onset seizures [> 4 days]
Long duration before starting treatment

258
Q

What are the immediate complications of bacterial meningitis?

A

Coma
Loss of airway reflexes
Seizures
Cerebral edema
Vasomotor collapse
DIC
Respiratory arrest
Dehydration
Pericardial effusion
Death

259
Q

What are the delayed complications of bacterial meningitis?

A

Seizure disorder
Focal paralysis
Subdural effusion
Hydrocephalus
Intellectual deficits
Sensorineural hearing loss
Ataxia
Blindness bilateral adrenal hemorrhage
Death

260
Q

Define Chronic meningitis

A

Meningitis lasting longer than a month without improvement

261
Q

What are the common causes of Chronic meningitis?

A

Chronic bacterial or fungal infections

TB
Cryptococcal
Syphilis
Cysticercosis
Lyme

262
Q

What conditions are commonly seen in patients with TBM?

A

Mild anemia
Hyponatremia
Subcortical strokes

263
Q

What is tuberculous vasculopathy?

A

A complication of TB

Multiple or bilateral lesions in territories of MCA perforating vessels

264
Q

What investigations must be done to diagnose TBM?

A

MRI
PPD [possible]
CSF analysis
↑ protein
↓ glucose
Lymphocytic pleocytosis
PCR
Culture

265
Q

Treatment for TBM?

A

Isoniazid
Rifampin
Pyrazinamide
Ethambutol
Dexamethasone [initial phase]

266
Q

What are the neurological sequelae associated with TB?

A

Developmental delay in children
Seizures
Hydrocephalus
CN palsies

267
Q

Prognosis of TBM?

A

Death in 50% of cases

268
Q

Mortality of TMB

A

Greatest in >5 yrs or 50 yrs< or illness longer than 2 months

269
Q

What are the causative microorganisms of brain abscess?

A

Streptococci [60-70%]
Bacteroides
Enterobacteriaceae
Staphylococcus aureus
S. milleri

270
Q

What are the rare causative microorganism of brain abscess?

A

Nocardia
Listeria

271
Q

What is the treatment for brain abscesses?

A

Ceftriaxone
Metronidazole [anaerobes]
Surgical drainage
[If >2.5 cm
If neurologically unstable
If decreased consciousness]

272
Q

What are the causes of subdural empyema?

A

Extension of sinusitis
Otitis media

273
Q

What is the treatment for subdural empyema?

A

Ceftriaxone
Metronidazole [anaerobes]
Surgical drainage

274
Q

What are the pain-sensitive intracranial structures?

A

Blood vessels [vasodilation is painful]
Meninges
Nerves

275
Q

What are the pain-sensitive extracranial structures?

A

Scalp
Joints
Muscles
Teeth, Eyes and Ears

276
Q

What is the prevalence of headaches?

A

96-99%
>90% are benign

277
Q

What are the 5 mechanisms of Headaches?

A

Traction on major vessels or meninges
Distension of arteries
Inflammation near pain-sensitive structures
Direct pressure on cranial arteries or cervical nerves
Sustained contraction of scalp/neck muscles

278
Q

How do you differentiate between primary and secondary headaches?

A

History [onset, severity, systemic features]

279
Q

What are the redflags for secondary headaches?

A

Systemic symptoms
Secondary risk factor
Neurological symptoms
Onset
Older age [new onset or progressive pain]
Pregnancy
Postural aggravation
Papilledema
Previous history of headache
Precipitated by valsalva

280
Q

What condition is associated with older onset of headaches ?

A

Giant cell arteritis

281
Q

What are some vascular causes of headaches?

A

Stroke
SAH
Intracerebral hemorrhage

282
Q

What are some infectious causes of headaches?

A

Meningitis
Sinusitis
Post-herpetic neuralgia

283
Q

What are some inflammatory causes of headaches?

A

Temporal arteritis

284
Q

What are some drug-related causes of headaches?

A

Nitrates
Caffeine withdrawal
Sympathomimetics

285
Q

What are some metabolic / systemic causes of headaches?

A

Anemia
Hypercalcemia
Renal Failure
Hypoxia
Hypercarbia

286
Q

What are some ophthalmologic causes of headaches?

A

Glaucoma
Ischemia

287
Q

What are some conditions that cause decreased ICP and headaches?

A

Post-Lumbar puncture
Spontaneous Intracranial hypotension

288
Q

What are some conditions that cause increased ICP and headaches?

A

Mass
Hypertension
Pseudotumor/Idiopathic Intracranial hypertension

289
Q

What are the primary headache disorders?

A

Migraine
Tension
TACs [Cluster, Paroxysmal Hemicrania, SUNCT and Hemicrania continua]
Others [Trigeminal Neuralgia and Occipital neuralgia

290
Q

What is associated with Migraines?

A

Nausea and Vomiting

291
Q

What type of migraine is common?

A

Without aura

292
Q

What is the severity of Migraine headaches?

A

Moderate to severe intensity

293
Q

What are the auras of migraines?

A

Photophobia
Phonophobia
Osmophobia

294
Q

What is the commonest aura of migraines?

A

Photophobia

295
Q

What are the complications of migraine?

A

Stroke
Seizures
Status migrainosus [>72hrs]
Chronic migraines
Persistent migraine w/o infarction

296
Q

What is the clinical presentation of Childhood Migraines?

A

Benign Paroxysmal Vertigo
Cyclic Vomiting
Abdominal migraines

297
Q

What is used to treat acute migraines?

A

Analgesia
Triptans

298
Q

How can we educate Migraine patients?

A

Avoid triggers
Diary documenting their headaches [timings, frequency, relation to menses]
Patients shouldn’t abuse analgesic treatments

299
Q

T/F: There are no preventative treatments for Migraines.

A

False, there are some preventative methods such as monoclonal antibodies against CGRB

300
Q

What is the commonest reported headache? Commonest primary headache?

A

Reported: migraine
Primary: Tension

301
Q

What are Tension headaches?

A

Tight band on the head

302
Q

What conditions are associated with Tension headaches?

A

Stress
Depression
Associated with medication-overuse headaches

303
Q

What is the severity of Cluster headaches?

A

Severe to very severe

304
Q

Describe the state of patient with Cluster headaches

A

Suicidal and unable to sleep

305
Q

What is the duration of Cluster headaches?

A

15-180 min

306
Q

What is used to treat Cluster headaches?

A

Abortive and prophylactic treatment [oxygen mask]

307
Q

What is the severity of Paroxysmal hemicrania?

A

Moderate pain

308
Q

What is used to treat Paroxysmal hemicrania?

A

Indomethacin

309
Q

What is the duration of Paroxysmal hemicrania?

A

2-30 minutes , episodic or chronic

310
Q

What type of headache is very rare and difficult to treat?

A

SUNCT headaches

311
Q

What does SUNCT stand for?

A

Short lasting
Unilateral
Neuralgiform headache w/
Conjunctival injection and
Tearing

312
Q

What is the duration of SUNCT headaches?

A

1-600 sec

313
Q

What is the severity of Hemicrania continua?

A

Mild to moderate pain

314
Q

What type of headache is associated with autonomic features?

A

Hemicrania continua and other TAC headaches

315
Q

What autonomic features are associated with TAC headaches?

A

Ptosis
Miosis
Facial swelling
Tearing
Nasal Congestion

316
Q

What is the duration of hemicrania continua headaches?

A

Continuous

317
Q

Define Neuralgia

A

Very sharp pain in seconds that can happen several times a day

318
Q

What structures are affected in Trigeminal Neuralgia?

A

Maxillary [V2] and Mandibular [V3] divisions of the trigeminal nerve [CN5]

319
Q

What is used to treat Trigeminal Neuralgia?

A

Carbamazepine

320
Q

What structure is affected in Occipital neuralgia?

A

C2- Occipital region of head

321
Q

Onset of AD?

A

>65 yrs.

322
Q

What pathological findings of AD?

A

Extracellularly: aB
Intracellularly: Tau

323
Q

What are the risks of AD?

A

Vascular
TBI
Sleep Disturbances
TREM2
ADOE E4 alleles

324
Q

What factors may reduce the risk of AD?

A

Increased formal education
Physical activities
Social engagement

325
Q

What is the hallmark findings of Early onset AD?

A

Disproportionately decreased repetition of sentences

326
Q

Presentation of Posterior Cortical Atrophy

A

Progressive and Disproportional loss of visuospatial and visuoperceptiual

327
Q

Differences of presentation of Early onset and Late onset Ad?

A

Early onset has better memory recognition score and semantic memory compared to late onset

328
Q

Pathological differences between Early onset and Late onset Ad?

A

Early onset: Posterior Cingulate

Late onset: Medial temporal lobe

329
Q

What is the second most common cause of Early-onset AD?

A

Posterior Cortical Atrophy

330
Q

What are the core clinical features of Lewy-body dementia?

A

Fluctuating cognition
Recurrent Visual Hallucination
REM Sleep Behaviors
Cardinal Features of Parkinsonisms

331
Q

What are the supportive clinical features of Lewy-body dementia?

A

Hypersomnia/Hyposomnia
Hallucination
Systemic Delusions
Apathy
Severe Autonomic Dysfunction
Repeated Falls/Postural Instability
Syncope
Severe sensitivity to Antipsychotic agents

332
Q

What is the hallmark of Delirium?

A

Acute impairment of cognition with fluctuating course

333
Q

Criteria for Delirium

A

Acute Onset + Fluctuating course

Inattention

Disorganized Thinking

Altered levels of Consciousness

334
Q

Criteria for Persistent Vegetative state?

A

1 month

335
Q

Criteria for Permanent Vegetative state?

A

3 months
6 months in TBIs

336
Q

What is the afferent limb for light reflex?

A

Optic nerve

337
Q

What is the efferent limb for light reflex?

A

Oculomotor nerve

338
Q

What findings are consistent with total loss of afferent limb of light reflex?

A

No direct or consensual reflex in affected eye

339
Q

What findings are consistent with partial loss of afferent limb of light reflex?

A

Partial constriction
Both eyes dilate

340
Q

Findings of Optic Neuritis

A

Central Scotoma
Optic Disc swelling [2/3 retrobulbar]

341
Q

Causes of Mydriasis?

A

CN 3 Palsy
Cocaine
Atropine

342
Q

Causes of Miosis?

A

Horner’s Syndrome
Tertiary Syphilis
Morphine
Pilocarpine

343
Q

Where is a lesion located if patient say he sees a “pie on the floor”?

A

Parietal lobe

344
Q

Where is a lesion located if patient say he sees a “pie in the sky”?

A

Temporal lobe

345
Q

Complete loss of vision in one eye

A

Optic nerve

346
Q

Bitemporal hemianopia

A

Optic Chiasma

347
Q

Homonymous Hemianopia

A

Optic tract

348
Q

UR Quadrant hemianopia

A

Lower fibers in temporal lobe

349
Q

LR Quadran hemianopia

A

Lower fibers in parietal lobe [anterior]

350
Q

Homonymous Hemianopia w/macular sparing

A

Lower fibers in parietal lobe [posterior]

351
Q

Lesion in Pontine/Midbrain would produce?

A

eyes deviate toward hemiparesis [wrong way gaze]
Vertical gaze [midbrain]
Abducent nerve [pontine]

352
Q

Lesion in Hemisphere would produce?

A

away from hemiparesis

353
Q

What structure is affected in Internuclear Opthalmoplegia?

A

MLF

354
Q

What are some causes of Internuclear Opthalmoplegia?

A

MS
Brainstem infarcts

355
Q

Findings in Internuclear Opthalmoplegia?

A

Side of lesion is the same side that fails to adduct:
1- Abduction [normal]
2-Adduction [eye on side of lesion fails to adduct]
3- Normal eye nystagmus
4- Affected eye fails to adduct

CNS (10 decks)

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