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MBBS VI Medicine > CNS system > Flashcards

CNS system Flashcards

1
Q

What is GCS components?

A
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2
Q

What to assess in the muscle tone of UL?

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3
Q

How is musle power graded?

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4
Q

What muscles and nerve roots control the shoulder, elbow, wrist and fingers?

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5
Q

What muscles do the median, radial and ulnar nerve control and their action?

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6
Q

What are the reflexes of the UL and their corresponding nerve origin?

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7
Q

What are the sensation landmarks of the upper limb?

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8
Q

How to test for coordination in lower limb
Differentiate between UMN lesion (pyramidal) and cerebellar lesion?

A
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9
Q

How to assess the muscle tone of the lower limb?

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10
Q

How to assess the muscle power of the lower limb their muscles and corresponding nerve root?

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11
Q

What are the LL reflexes and their nerve origin?

A
  • Knee jerk: L3 – 4
  • Ankle jerk: S1 – 2
  • Plantar jerk (Babinski’s sign): L5 – S2
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12
Q

What are the sensation landmarks of the lower limb?

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13
Q

How to test the coordination of the lower limb
Loss of proprioception?
How to assess the gait?

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14
Q

What are the functions of CN1-5 and their clinical findings on CN palsy?

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15
Q

What are the functions of CN6-9 and their clinical findings on CN palsy?

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16
Q

What are the functions of CN10-12 and their clinical findings on CN palsy?

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17
Q

How to assess the optic nerve?

A
  • Visual acuity: only 1 eye tested each time. Test with patient wearing his or her spectacles.Refractive errors are not considered to be CN abnormalities
    Test with snellens chart at 1 arms length.
    If unable to read –> count fingers –> hand movement –> light perception –> no perception of light (blind)
  • Assessment of pupil size
    Physiologic anisocoria: difference <0.4mm
    Anisocoria greatest in bright light = larger pupil is affected. Indicates poor pupillary constriction on the abnormal side. Indicates abnormality of parasymp system
    Anisocoria greatest in dim light = smaller pupil is affected. Indicates poor pupillary dilatation on the abnormal side. Indicates an abnormality of the symp system

Pupillary light reflex. Direct response: pupillary constriction of the stimulated eye. Consensual response –> pupillary constriction of unstimulated eye

RAPD
Normal RAPD test: relative dilatation of pupil when light shone on the affected eye
Reverse RAPD test performed in patients with unreactive pupils: relative dilatation of the contralateral eye when light shone on the affected eye
ddx of RAPD
Optic nerve: optic neuritis, optic atrophy (glaucoma), ischemic optic neuropathy/compressive or traumatic optic neuropathy
Retina: CRAO/BRAO/CRVO/BRVO/retinal detachment

Accomodation reflex
Light near dissociation is tested by accomodation reflex: accomodate but not react to light
ddx of light near dissociation: argyll robertson pupil (syphilis/DM autonomic neuropathy), Adies tonic pupil

Visual field

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18
Q

What is the function of CN3,4,6 and what is innervated?

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19
Q

Compare medical vs surgical CN3 palsy and its presentation and cause

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20
Q

What is the causes of CN3 palsy based on anatomical location?

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21
Q

Causes of CN4 palsy by laterality
By anatomical location

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22
Q

Causes of CN6 palsy by anatomical location

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23
Q

What to assess in ptosis and the underlying types (ddx)?

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24
Q

How to differentiate the type of diplopia?

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25
Q

What is the pathophysiology of nystagmus
The types, causes and features?

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26
Q

What structure and pathway is involved in the horizontal gaze?

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27
Q

What are the causes of horizontal gaze disturbances?

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28
Q

What are the causes of vertical gaze disturbances?

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29
Q

How to do PE of CNV?
Causes of CNV palsy?

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30
Q

What muscles involved in CN7
What affects UMN and LMN and difference in clinical presentation for UMN and LMN?

A
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31
Q

How to test the function of CN8 and its results?

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32
Q

What are the causes of conductive deafness (outer ear and middle ear)?

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33
Q

What are the causes of sensorineural deafness ?

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34
Q

How to examine CN9,10 and the causes of these palsies?

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35
Q

How to examine CN11
Causes of CN11 palsy?

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36
Q

How to examine CN12
Causes of CN12 palsy?

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37
Q

Compare bulbar and pseudobulbar palsy in casues, jaw jerk, gag reflex, speech, tongue and emotions

A
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38
Q

Localization of lesion in the spinal cord?

A
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39
Q

What is normal range of ICP
What is ICP?

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40
Q

What are the causes of increased ICP?

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41
Q

What regulates cerebral perfusion pressure and cerebral blood flow?

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42
Q

What is the cerebral autoregulation in hypertension?

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43
Q

What are the SS of increased ICP?

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44
Q

What are the cerebral herniation syndromes?
What signs will they have?

A
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45
Q

What are the indications for ICP monitoring and the method done?

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46
Q

What is general management of increased ICP?

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47
Q

What is the treatment of increased ICP?

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48
Q

Define hydrocephalus

A

Disorders in which excessive amount of CSF accumulates within cerebral ventricles or subarachnoid spaces which are dilated

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49
Q

How to classify hydrocephalus?

A

 Obstructive (non-communicating) hydrocephalus
* Obstruction in CSF circulation leading to accumulation of CSF in cerebral ventricles
 Communicating hydrocephalus
* Impaired absorption of CSF leading to accumulation of CSF in cerebral ventricles

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50
Q

How is the production of CSF and pathway done?

A
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51
Q

What is the pathogenesis of hydrocephalus?

A
  • Increased CSF production: choroid plexus papilloma
  • Decreased CSF absorption: bacterial meningitis (leads to arachnoid granulation adhesions)
  • Obstruction of CSF flow: aqueductal stenosis, tumor
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52
Q

What is the clinical manifestation of hydrocephalus?

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53
Q

What is treatment of hydrocephalus?

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54
Q

What are the SS of Horner syndrome?

A

Interruption of sympathetic nerve pathway to the eye and face

 Partial ptosis: Paralysis of Muller’s (superior tarsal) muscle which is innervated by sympathetic pathway and levator palpebrae superioris being unaffected
 Miotic reactive pupil: Anisocoria with abnormal small pupil in the dark and associated dilation lag
 Enophthalmos: NOT a true enophthalmos and occurs as an illusion due to ptosis and updrawing of lower
eyelid which together narrows the palpebral fissure
 Anhidrosis: Loss of sympathetic fibers for facial sweating and vasodilation

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55
Q

What are the causes of Horner syndrome (1st order, 2nd order and 3rd order)?

A
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56
Q

What is the sympathetic pathway of Horner syndrome?

A
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57
Q

What are the Ix done to confirm the dx of Horner syndrome?

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58
Q

Define delirium

A

Acute confusional state characterized by global cognitive dysfunction and inattention
* Confusional state refers to state of altered consciousness with disorder attention along with diminished speed, clarity and coherence of thought

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59
Q

What are the precipitating factors for delirium?

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60
Q

What is the pathophysiology of delirium?

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61
Q

What are the SS of delirium?
What are associated features?

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62
Q

What is the ddx for delirium?

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63
Q

What is the diagnostic criteria for delirium?

A

DSM-V

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64
Q

What is the history taking for delirium?

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65
Q

What is the PE done for delirium?

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66
Q

What are the basic blood tests done for delirium?

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67
Q

What imagings and non basic Ix may be done for delirium?

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68
Q

What is general management and medical management for delirium?

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69
Q

What are the general features of coma?

A

 Defined by unarousable unresponsiveness
 Medical emergency characterized by absence of consciousness
* Consciousness requires arousal (awake) and awareness (have content)
 Timely identification and treatment of reversible cause can be life-saving
 Caused by structural brain lesions, diffuse neuronal dysfunction or psychiatric illnesses

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70
Q

What are the levels of consiousness?

A
  • Vigilant = Hyperalert
  • Normal = Alert
  • Lethargy = Drowsiness but easy to arouse
  • Stupor = Difficult to arouse
  • Coma = Unarousable
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71
Q

What are the tests for certifying brain death?

A
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72
Q

What is the system involved with consiousness?

A

 Ascending reticular activating system (ARAS)
* Network of neurons originating in the tegmentum of upper pons and midbrain
* Neurons project to thalamus and hypothalamus and subsequently to cerebral cortex
* Responsible to induce and maintain alertness
o Injury to ARAS with upper brainstem or cerebral hemispheres by focal lesions can cause alteration in consciousness

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73
Q

What are the symmetrical structural causes of coma (supratentorial and infratentorial)?

A
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74
Q

What are the asymmetrical structural causes of coma (supratentorial and infratentorial)?

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75
Q

What are the symmetrical non structural causes of coma?

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76
Q

What are the conditions mistaken for coma?

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77
Q

What initial assessment for coma patient?
What is history taking?

A
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78
Q

What is done for PE of coma patient?

A

Must look out for reversible causes and treat promptly

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79
Q

What are the biochemical tests done for coma patients?

A
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80
Q

What imaging and non blood Ix done for comatose patient?

A

 ABG/ VBG
 CXR
 ECG
 EEG
 CT brain
 CT angiography
 MRI venography

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81
Q

What is the initial stabilization management of comatose patient?
What is supportive care?

A
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82
Q

What are the red flags of headache in adults?

A
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83
Q

What is the history taking of headache?

A
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84
Q

What is the PE for headache?

A
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85
Q

What is the ddx of headache depending on timeline, patient demographic and associated conditions (i.e. fever, immunocompromised, traumatic brain injury)

A
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86
Q

What is migraine associated with
Classification of migraine
Precipitating factors of migraine (descending order)

A
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87
Q

What are the genetics involved in migraine?

A
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88
Q

What is the pathophysiology of migraine?

A
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89
Q

What is the clinical manifestation of migraine (4 phases)?

A
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90
Q

What is the diagnostic criteria for migraine without aura?

A

ICHD-3

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91
Q

What is the diagnostic criteria for migraine with aura?

A

ICHD-3

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92
Q

When may imaging be indicated for headache?

A
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93
Q

What is the treatment for migraine?

A
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94
Q

What is done for prevention of migraine?

A

 β-blockers
* Propranolol
* Metoprolol
* Timolol
 Anti-depressants
* Amitriptyline (TCA)
* Venlafaxine (SNRI)
 Anti-convulsants
* Topiramate
* V alproate

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95
Q

What is general feature of tension type headache?
Classification of TTH?
Precipitating factors of TTH?

A
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96
Q

What is pathophysio of tension type headache?

A

 Peripheral factors
* Peripheral activation or sensitization of myofascial nociceptors
* Associates with pericranial muscle tenderness
 Central factors
* Sensitization of pain pathways in CNS due to prolonged nociceptive stimuli from pericranial myofascial tissues

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97
Q

What is clinical manifestatin of tension type headache?
What is the specific PE done?

A
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98
Q

What is the diagnostic criteria for episodic and chronic TTH?

A

ICHD-3 (international classification of headache disorders-3rd edition)

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99
Q

What is done for treatment of tension type headache
What prevention management

A
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100
Q

What is the clinical manifestation of cluster type headache?

A
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101
Q

What is cluster type headache
What proposed theory for pathophysiology?

A

 Belongs to an idiopathic headache entity known as trigeminal autonomic cephalalgias (TACs)
 Severe unilateral headache typically accompanied by autonomic symptoms

 Theory 1: Hypothalamic activation with secondary activation of trigeminal-autonomic reflex through a trigeminal-hypothalamic pathway
 Theory 2: Neurogenic inflammation of walls of cavernous sinus obliterates venous outflow
* Leads to injury of traversing sympathetic fibers of the intracranial ICA and its branches

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102
Q

What is the diagnostic criteria for episodic cluster headache and chronic cluster headache?

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103
Q

What is treatment and prevention of cluster type headache

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104
Q

What is general feature of trigeminal neuralgia
What is the etiology?

A

 Recurrent brief episodes of unilateral electric shock-like pains that is abrupt in onset and offset
 Located in the distribution of one or more divisions of CN V

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105
Q

What is clinical manifestation of trigeminal neuralgia?

A
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106
Q

What is diagnostic criteria for trigeminal neuralgia?
What radiological Ix may be indicated and why?

A
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107
Q

What is medical treatment for trigeminal neuralgia
What is surgical treatment (refractory to medical treatment)?

A
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108
Q

What is giant cell arteritis (temporal arteritis)?
What associated condition?
Is it a medical emergency?

A

Chronic systemic vasculitis involving large and medium sized arteries: aorta and great vessels. Commonly affects the temporal and other cranial arteries originating from the aortic arch

Strongly associated with polymyalgia rheumatica in 40-60% of patients. Characterized by pain and morning stiffness around shoulder and hip girdles, neck as well as in the torso. However GCA only found in 15% of patients with PMR.
Medical emergency (amourosis fugax) du to cranial arteritis without early detection and treatment

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109
Q

What is epidemiology of giant cell arteritis
RF
Pathogenesis

A
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110
Q

What is the SS of giant cell arteritis?

A
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111
Q

What is diagnostic criteria for temporal arteritis (giant cell arteritis)
What biochemical tests should be done to make dx

A
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112
Q

What is early treatment of temporal arteritis?

A
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113
Q

What are the main cerebral arteries?

A
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114
Q

What are the anatomical locations of intracranial aneurysms?

A

 Most subarachnoid hemorrhage are caused by ruptured intracranial saccular (berry) aneurysm
 Anatomical location of intracranial aneurysm
* Anterior circulation (85%)
o Bifurcation of MCA
o Junction of ACA and anterior communicating artery
o Junction of ICA and posterior communicating artery
* Posterior circulation (15%)
o Top of basilar artery
o Junction of basilar artery and superior cerebellar artery
o Junction of basilar artery and anterior inferior cerebellar artery
o Junction of vertebral artery and posterior inferior cerebellar artery

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115
Q

What are the RF for cerebral aneurysms?

A
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116
Q

What is the different types of aneurysm?

A

 Saccular (berry) aneurysm: Thin-walled protrusion from intracranial arteries that composed of a very thin or absent tunica media and a severely fragmented or absent internal elastic lamina
 Fusiform aneurysm: Enlargement or dilatation of entire circumference of the involved vessel that may in part be formed due to atherosclerosis
 Mycotic aneurysm: Result from infected emboli due to infective endocarditis

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117
Q

What is the clinical manifestation of cerebral aneurysm (unruptured and ruptured)?

A
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118
Q

What are imagings for cerebral aneurysm?

A

 General features
* Most intracranial aneurysms are incidental findings
 Imaging modalities
* CT angiography
* MRI angiography
* Cerebral angiography

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119
Q

What are the indications for intervention of cerebral aneruysm?
What surgical treatment options are there?

A
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120
Q

What subtypes of congenital vascular malformations of CNS are there?

A
  • AVM: possible neurological sequelae (most dangerous)
  • Cavernous malformation (cavernous angioma): possible neurological sequlae
  • Developmental venous anomalies (venous angioma); more benign
  • Capillary telangiectasia: more ebenign
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121
Q

Describe the different cerebral vascular malformations

A
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122
Q

What is clinical manifestation of AVM?

A
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123
Q

What are the imaging Ix for cerebral vascualr malformatino?

A
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124
Q

What is the grading scale for intracranial AVMs?
What surgical treatment options are there?

A
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125
Q

What is classification of stroke?

A
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126
Q

Define transient ischemic attack?
What is the scoring system for assessing whether patient should be admitted into hospital?

A
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127
Q

What are the causes of ischemic stroke (thrombosis) –> large vessel (intracranial, extracranial, small vessel intracranial)?

A
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128
Q

What are the ischemic stroke causes (embolism) cardiac and aortic source?

A
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129
Q

What are the ischemic stroke causes systemic hypoperfusion?

A
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130
Q

What are the ischemic stroke causes (hypercoagulability)?

A
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131
Q

What are the causes of hemorrhagic stroke?

A
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132
Q

What is pathological appearance of stroke?

A

 Pale infarction which is swollen and slightly softened
* Blood cannot reach the area distal to obstruction and thus pale in appearance
 Hemorrhagic infarction
* Reperfusion to ischemic part of the brain will lead to hemorrhagic appearance
o Capillaries are damage during ischemia and can no longer stand the BP when blood flow is reestablished
 Cracking and liquefactive necrosis
 Resorption with replacement by fluid filled cavities

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133
Q

What is the histological appearance of stroke?

A
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134
Q

What are cortical signs indicative of cortical stroke (ischemic)?

A
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135
Q

What are subcortical signs indicating location of ischemic stroke?

A
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136
Q

What areas of the brain does the ACA supply
What would be the clinical manifestation if affected?

A
137
Q

What areas of the brain does the MCA supply
What would be the clinical manifestation if affected?

A
138
Q

What areas of the brain does the PCA supply
What would be the clinical manifestation if affected?

A
139
Q

What areas of the brain does the basilar artery supply
What would be the clinical manifestation if affected?

A
140
Q

What areas of the brain does the vertebral artery supply
What would be the clinical manifestation if affected?

A
141
Q

What is lacunar syndrome and what are the types?
What artery is affected?

A

Lenticulostriate arteries (branch of MCA)

142
Q

What is the ddx for ischemic stroke?

A
143
Q

What is history taking for stroke?

A
144
Q

What is done for PE stroke?

A

Always assess vitals and resuscitate if necessary
Locate the lesion from high to low: cortical signs –> CN –> UL, LL (muscle tone, power, reflex, sensation, vibration and proprioception) cerebellar signs

145
Q

What are the biochemical tests for stroke and why are they done?

A
146
Q

What are the imagings done for stroke?

A

DSA for smal aneurysm as cause of SAH and if non invasive studies are inconclusive (invasive intracranial vascular study)

147
Q

What are non contrast CT scan early signs of infarction?

A

o Focal parenchymal hypoattenuation
o Hypoattenuation involving ≥ 1/3 MCA territory
o Hyperattenuation of large vessels (e.g. MCA occlusion)
(“Dense MCA sign” which does not respond well to IV tPA)
o Cortical sulcal effacement
o Loss of gray-white differentiation in basal ganglia
o Loss of insular ribbon
o Obscuration of lentiform nucleus
o Obscuration of Sylvian fissure

148
Q

What is the general management of ischemic stroke patients?

A
  • Airway: airway support and ventilatory support if decreased consiousness or who have bulbar dysfunction that causes airway compromise
  • Breathing: supplemental O2 therapy taht should be provided to maintain sO2 >94%. Not reommended in non hypoxic patients
  • Circulation: BP. Target BP <185/110mmHg. BP should be maintained at <180/105mmHg for at least 24 hours after fibrinolytic therapy
    Patients not eligable for fibrinolysis: BP should not be treated acutely (permissive hypertension) unless hypertension is extreme as defined by >220/120mmHg, careful lowering of BP by about 15% in the first 24 hours after stroke is recommended. BP carefully lowered as it may be necessary to maintain cerebral blood flow to ischemic brain regions.
  • Body temp: source of hypothermia should be identiied and treated. Antipyretic medication should be administered to lower temp in hyperthermic patients with stroke
  • Blood glucose level: hyperglycemia (associated with worse outcomes) –> target BG = 7.8-10mmol/L. Hypoglycemia with serum glucose <3.33mmol/L should be treated
  • Diet and nutrition: enteral diet should be started within 7 days of admission (avoid acalculous cholecystitis), swallowing assessment to screen for dysphagia before initiating any oral intake –> dysphagia increases chance of aspiration pneumonia. NG tube feeding reasonable for patients with dysphagia in early phase of stroke. PEG tubes for longer anticipated patients.
  • Positioning and splinting to avoid aspiration, contractures, pressure nerve palsy, shoulder subluxation and pressure sores
  • Avoid bladder overdistension and UTI with catheterization
  • Avoid constipation or fecal impaction by high fiber diet and stool softeners
149
Q

What is medical treatment for ischemic stroke?

A
150
Q

What are the contraindications for fibrinolytic therapy in ischemic stroke?

A
151
Q

What are the complications for fibrinolytic therapy in ischemic stroke?

A
152
Q

Are antiplatelets and anticoagulants give in ischemic stroke?

A

Antiplatelets: recommended to initiate within 24-48 hours of onset of acute ischemic stroke. Dosage = 160-325mg once daily
Should be delayed until 24 hours later if IV alteplase (tPA) is given since increase risk of symptomatic ICH and may not improve functional outcome

Anticoagulants are recommended against being used
Only indicated if cardiogenic embolism for secondary prevention of stroke in patients with AF, DVT or PE, cerebral venous thrombosis

153
Q

What is the surgical management for ischemic stroke?
What is the cut off time for eligability of surgical intervention?

A
154
Q

What are acute and chronic complications in acute ischemic stroke and how are they managed?

A
155
Q

What is the general management of hemorrhagic stroke?

A
156
Q

What is medical management of hemorrhagic stroke?

A
157
Q

What is surgical management of intracerebral hemorrhage?

A
158
Q

What is the surgical treatment for subarachnoid hemorrhage?

A
159
Q

What are treatment of acute complications of hemorrhagic stroke?
Treatment of potential chronic complications?

A
160
Q

What is the secondary prevention management of ischemic stroke?

A
161
Q

How to prevent vasospasm in cerebral aneurysm?

A

 Nimodipine
* CCB to prevent vasospasm
* Administered to ALL patients with aneurysmal subarachnoid hemorrhage

162
Q

What are the complications of stroke?

A
163
Q

What is done for stroke rehabilitation?

A
164
Q
  1. dx
  2. Expected CT findings
  3. Common RF for cererbal infarction
A
  1. Cerebral infarction/hemorrhage at subcortical regiion
  2. Infarction (hypodense lesion), hemorrhage (hyperdense lesion)
  3. HT, DM, smoking, HL, strong FH of strokes
165
Q

What are the diagnosis and on what grounds are they made?

A

 CVS system
* Mixed mitral valve disease
* Pulmonary hypertension
* Atrial fibrillation
 CNS system
* Wernicke’s aphasia from a cardioembolic stroke
o Posterior part of the left superior temporal gyrus
o Supported by the history of reduced exercise tolerance, palpitation (AF), mixed mitral valve disease and sudden onset of fluent aphasia

166
Q

Wernickes aphasia from a cardioembolic stroke
What suggests this dx on PE?

A

 CVS system
* Pan-systolic murmur at apex radiating to axilla suggest mitral regurgitation
* Mid-diastolic murmur with postural accentuation suggest mitral stenosis
* Irregular pulse with higher apical rate than pulse suggest atrial fibrillation
* Parasternal heave and loud pulmonic component of S2 suggest pulmonary hypertension
 CNS system
* Fluent aphasia with normal neurological examination suggest stroke affecting Wernicke’s
area

167
Q

Clinically how do you determine the severity of mitral stenosis versus mitral regurgitation in patients with mixed mitral valve disease?

A

 Features suggesting predominant mitral stenosis
* Small volume pulse
* Undisplaced tapping cardiac apex
* Long diastolic murmur
* Pulmonary hypertension
 Features suggesting predominant mitral regurgitation
* Displaced cardiac apex
* Palpable systolic thrill

168
Q

Where is the Wernicke’s area?

A

 Posterior part of the left superior temporal gyrus
 Lesion involving this area will lead to Wernicke’s (receptive) aphasia

169
Q

What is the classification of subdural haematoma?

A
170
Q

Compare epidural and subdural hemorrhage by etiology, cross suture, cross midline, clinical course, clinical manifestation and CT findings

A

Epidural can also be caused by traumatic injury to head via veins in the scalp

171
Q

What are causes of epidural haematoma?

A
172
Q

What are causes of subdural haematoma?

A
173
Q

What are the different layers of the dura?

A
174
Q

What is injured in epidural haematoma?

A

If penetrating trauma can be scalp vein

175
Q

What is injured in subdural haematoma?

A
176
Q

What are SS of subdural/epidural hemorrhage?

A
177
Q

What imaging done for epidural/subdural hemorrhage?

A
178
Q

What is management of epidural and subdurla haematoma?

A
179
Q

What is the distribution of types of brain tumors?

A
180
Q

What is epidemiology of brain tumors in paeds?

A

Primary malignant CNS tumours are the 2nd most common childhood malignancy after hematological malignancy
* Most common pediatric solid organ tumour
* Highest mortality from childhood cancer surpassing ALL
* Highest morbidity from childhood cancer primarily neurological deficits

181
Q

4 MOST common types of brain tumours in children in HK

A
  • Astrocytoma/ Other gliomas
  • Primitive neuroectodermal tumours (PNETs) including medulloblastoma
  • Germ cell tumours (GCTs) (Asians: Caucasians = 6:1)
  • Ependymoma
182
Q

What are the sites of CNS tumors in children?

A
183
Q

What is the general epidemiology of brain tumors affecting children?

A
184
Q

What are the associated familial syndromes associated with brain tumors?

A
185
Q

What forms the anterior border of the posterior cranial fossa?

A
186
Q

What are symptoms for brain tumors based on location
Supratentorial
Infratentorial (posterior fossa)
Spinla cord
Other structures (hypothalamus/pituitary, pineal gland, optic pathway)

A
187
Q

What are general SS for brain tumors?

A
188
Q

What are focal SS of brain tumor?

A
189
Q

What are cerebellar signs?

A
190
Q

What are SS of increased ICP?

A
191
Q

What is the classification of astrocytomas?

A
192
Q

What is the most common type of malignant CNS tumors of childhood?

A

Primitive neuroectodermal tumors (PNETs)(embyronal tumors)

193
Q

What is the WHO classification of intracranial germ cell tumors?

A
194
Q

What is the epidemiology for intracranial germ cell tumors
Clinical manifestation (pineal gland tumors, suprasellar tumors)

A
195
Q

How to make a dx of intracranial germ cell tumor?

A
196
Q

What is treatment for intracranial germ cell tumors?

A
197
Q

Where does ependymoma occur mostly
Affects what age group
Clinical manifestation

A
198
Q

What ix for brain tumors

A

Biochemical tests
CSF analysis by lumbar puncture
Tumor markers: AFP and B-hCG for GCTs. CSF cytology may reveal neoplastic cells which metastasize through CSF pathways

Radiological tests
CT brain: used for emergency situation. Detectin of metastasis to skull base, clivus or regions near foramen mangum
MRI brain: with and without contrast is neuroimaging standard. Superior to CT scan for evaluation of leptomeninges, subarachnoid space, posterior cranial fossa and defining vascualr distribution of the abnoramlity
* Perfusion MRI: imaging of blood flow in brain tumors with gadolinium in dynamic contreast MRI
* Functional MRI: preop planning for patients whose tumor is located near eloquent areas of the brain.
PET scan: detects malignant tumors with high metabolic rates. Localize areas of maxium glucose utilization within the tumor which guides biopsy of tumor location with most aggressive biological behaviour
SPECT scan: utilizes isotopes such as thallium-201 to detect abnormalities in BBB –> distinguish benign from malignant brain lesions, predict histological grade of brain tumors, select aeras for biopsy
Surgical exploration and biopsy: histological confirmation obtained at time of surgical exploration for resection

199
Q

What is medical and surgical treatment options for medulloblastoma?

A
200
Q

What is the mechanism of MG?
Types of MG

A
201
Q

What are the associated conditions with MG?

A
202
Q

What is the general epidemiology of MG?

A

 Bimodal distribution
* Early peak in 2nd and 3rd decades (female predominance)
* Late peak in 6th – 8th decades (male predominance)

203
Q

What is the pathogenesis of MG?

A
204
Q

What is SS of MG?

A
205
Q

What is ddx of MG?

A
206
Q

What is the PE for MG?

A
207
Q

What are the Ix for MG?

A
208
Q

What is medical and surgical treatment for MG?

A
209
Q

How to manage myasthenia crisis?

A
210
Q

How to prevent MG?

A

 Avoid drugs that unmask or exacerbate MG
* Antibiotics
o Fluoroquinolones
o Aminoglycosides
* CVS drugs
o β-blockers
o Procainamide
o Quinidine
* Others
o Penicillamine
o Magnesium sulphate
o Chloroquine
o Hydroxychloroquine

211
Q

Q1: After 6 months of mestinon (i.e. pyridostigmine) at 30 mg tds, she noticed increased proximal muscle weakness and moderate dysphagia. How do you manage her?
Q2: What are the non-drug alternatives for MG?

A

 Mestinon dose should be stepped up for inadequate response
 Systemic corticosteroids and steroid sparing drugs such as azathioprine are NOT started
* Due to concern of potential long-term adverse effects including lymphoproliferative diseases and teratogenicity in a young woman of child-bearing age

 Thymectomy
* Significant improvement can occur in the absence of a thymoma
 Plasmapheresis
* Used in intractable cases
* Benefit is temporary

212
Q

Compare myasthenia gravis and lambert eaton syndrome

A
213
Q

What are the other causes of ptosis apart from MG and how can they be differentiated?

A

 CN III palsy
* Usually complete ptosis
* Ophthalmoplegia
* Dilated unreactive pupil
 Horner’s syndrome
* Partial ptosis
* Miotic reactive pupil
* Anhydrosis (Failure of sweat glands)
* Enophthalmos (Posterior displacement of eyes)

214
Q

What is the disease pattern of multiple sclerosis?

A
215
Q

What is general feature of multiple sclerosis?

A

Most common immune-mediated inflammatory demyelinating disease of CNS
* Demyelination of the PNS by definition is NOT considered MS
* Demonstrates lesion disseminated in time and space

216
Q

What is the ddx of multple sclerosis?

A
217
Q

How is conjugate horizontal gaze to the right done?

A
  • Voluntary gaze to the right is initiated in the left cerebral hemisphere
  • Left cerebral hemisphere innervates right paramedian pontine reticular formation (PPRF) which is the horizontal gaze centre in pons
  • Innervates CN VI (abducens nerve) and thus lateral rectus muscle of right eye to abduct the right eye
  • Innervate CN III (oculomotor nerve) and thus medial rectus muscle of left eye to adduct the left eye via medial longitudinal fasciculus (MLF)
218
Q

What is the pathogenesis fo MS?
What are the pathological features?

A
219
Q

What is the clinical course of multiple sclerosis?

A
220
Q

What are the eye abnormalities in multiple sclerosis?

A
221
Q

What are sensory and motor symptoms of multiple sclerosis?

A
221
Q

What are autonomic symptoms of multiple sclerosis?

A
222
Q

What are the other systemic signs of multiple sclerosis?

A
223
Q

What is the diagnostic criteria for multiple ssclerosis?

A
224
Q

What are the Ix for multiple sclerosis?

A

Dawson fingers are a radiographic feature of demyelination characterised by periventricular demyelinating plaques distributed along the axis of medullary veins, perpendicular to the body of the lateral ventricles and/or callosal junction. This is thought to reflect perivenular inflammation. They are a relatively specific sign for multiple sclerosis.

225
Q

What are the disease modifiying treatment for multiple sclerosis?
Injectable therapies
Infusion therapies
AE of the above drugs

A
226
Q

What are the disease modifiying treatment for multiple sclerosis?
Oral therapies
AE of the above drugs

A
227
Q

What is Guillain-Barre syndrome?

A

 Acute immune-mediated progressive polyneuropathy characterized by a monophasic paralyzing illness provoked by a preceding infection
 Recognized as a heterogeneous syndrome with variant forms of distinguishing clinical, pathophysiological and pathological features

228
Q

What are the GBS variants?

A
229
Q

What are the precipitating factors of GBS?

A

 Preceding infections
* Bacterial: Campylobacter jejuni/ Mycoplasma pneumoniae
* Viral: CMV/ EBV/ VZV/ HIV/ Zika virus
 Recent vaccination
 Surgery
 Bone marrow transplant

230
Q

What is the pathogenesis of GBS?

A
231
Q

What is the clinical course of GBS?

A

 Monophasic illness pattern
* Progresses over a period of about 2 weeks
* Clinical symptoms reach a plateau (nadir) in 4 weeks

232
Q

What is the SS of GBS?

A
233
Q

What is the ddx of GBS?

A
234
Q

What is the diagnostic criteria for GBS?
Supportive features?
Features regendering dx of GBS doubtful?

A
234
Q

What biochemical tests for GBS?

A
235
Q

What non basic Ix for GBS?

A
235
Q

What is treatment for GBS?
What must be monitored

A
236
Q

What is the general features of ALS?

A
237
Q

What is the spectrum of motor neuron disease (ALS)?

A
238
Q

What is the ddx for ALS?

A
239
Q

What is pathophysiology of ALS?

A

 UMN lesions
* Result from degeneration of frontal motor neurons located in motor strip (Brodmann area 4) and their axons traversing corona radiata, internal capsule, cerebral peduncles, pontine base, medullary pyramid and lateral corticospinal tract
 LMN lesions
* Result from degeneration of lower motor neurons in brainstem and spinal cord producing muscle denervation

239
Q

What is SS of ALS?

A
240
Q

In ALS what is its effect on sensory function, cognitive function and extraocular movements?

A
241
Q

What is the diagnostic criteria of ALS?

A

Revised EI Escorial criteria

242
Q

What Ix done for ALS?

A
243
Q

What treatment for ALS?
What is prognosis?

A
244
Q

What is general features of poliomyelitis?

A

 Enteroviral infection that causes meningitis, prolonged or permanent flaccid paralysis or death
 Eradicated from most of the world due to mass vaccination

245
Q

What is cause of poliomyelitis?

A
246
Q

What is ddx of acute flaccid paralysis?

A
247
Q

What is pathogenesis of poliomyelitis?

A

 Virus replicates initially in the throat and intestine
 Disseminated via blood or lymphatic system
 Invades the central nervous system (CNS)
* Travel by anterograde axonal flow along peripheral nerves to spinal cord
* Viral replication then occurs in the motor neurons
* Leads to death of motor neurons leading to flaccid paralysis

248
Q

What is clinical manifestation of poliomyelitis?

A
  • Flu like syndromes
  • Aseptic meningitis
  • Paralytic poliomyelitis (0.1-1% of cases)
    Spinal poliomyelitis: starts with severe myalgia which is accompanied by muscle spasms, fasciculation and paresthesia. Followed by flaccid paralysis –> usually asymmetrical. Proximal muscle involvement >distal muscle involvement
    Bulbar poliomyelitis: result of paralysis of muscle groups innervated by the cranial nerves: CN9 and 10 most commonly involved nerve –> dysphagia and pooling of oral secretions. Involvement of resp center of medulla oblongata leads to resp muscle paralysis
249
Q

What is PE and ix done for poliomyelitis?

A
250
Q

What is treatment and prevention of poliomyelitis?

A
251
Q

What is the staging model for parkinsons disease?

A

Modified Hoehn and Yahr staging of Parkinsons disease

252
Q

What is the causes of parkinsons disease?

A
253
Q

What are the parkinsons plus syndrome types?

A
254
Q

What are causes of secondary parkinsonism?

A
255
Q

What is the pathophysio of Parkinsons disease?

A
256
Q

What is pathology of Parkinsons disease?

A

 Depigmentation, neuronal loss and gliosis in substantia nigra pars compacta in midbrain and locus ceruleus in pons
 Presence of Lewy bodies
* Pathological hallmark of PD but not specific to PD (e.g. Dementia with Lewy bodies)
* Lewy bodies are round eosinophilic intracytoplasmic neuronal inclusions which is made up of α-synuclein and ubiquitin

257
Q

What are the cardinal signs of Parkinsons disease?

A

TRAP

258
Q

What are other motor features apart from TRAP for Parkinsons disease?
Other non motor features?

A
259
Q

What are signs and gait for Parkinsons disease?

A
260
Q

What is the diagnostic criteria for Parkinsons disease?

A
261
Q

What are red flags (potential signs of alternative pathology) for Parkinsons disease?
What are absolute exclusion criteria (completely rule out PD)?

A
262
Q

What is PE and Ix done for Parkinsons disease?

A
263
Q

What is treatment for Parkinsons disease?
What are AE of drugs?

A
264
Q

Define seizure vs convulsion

A

 Seizure = Transient neurological symptoms due to abnormal excessive or synchronous neuronal activity which can be provoked or unprovoked
 Convulsion = Generalized tonic-clonic seizure

265
Q

Define acute symptomatic seizure (provoked seizure)

A
  • Defined as those occurring up to several weeks (up to 2 – 4 weeks) after the event
  • Provoked seizure that are NOT expected to recur in the absence of provocation
  • Transient factors that temporarily lower the seizure threshold
266
Q

Define epilepsy

A
267
Q

Define status epilepticus

A

Medical emergency
Can be convulsive (tonicclonic) or non convulsive: non convulsive SE refers to alteration of awareness ranging from confusion to coma without motor manifestation of seizure (diagnosed with EEG)
Definition: continous seizure lasting for >5 mins, >2 epilepitc seizures without full recovery of consiousness between attacks

268
Q

Define epilpeys syndrome?

A
  • Syndrome defined by a distinctive combination of clinical features, signs and symptoms and electrographic (EEG) patterns
  • Epilepsy syndrome classification provides genetic, therapeutic and prognostic values
  • Examples
    o Juvenile myoclonic epilepsy
    o Genetic epilepsy with febrile seizures plus (GEFS+)
269
Q

What are the causes of acute symptomatic seizure (50%)?

A
270
Q

What are the causes of epilepsy?

A
271
Q

What is ddx for syncope?
What questions need to be assess in history taking?

A
  • Syncope: prodrome (lightheadedness, nausea, visual blurring)
  • Seizure (aura, TLOC, convulsion, tongue biting, urinary incontinence, post ictal state (headache, confuson, fatigue, muscle sores…)
  • TIA (hemiparesis and hemisensory loss, aphasia in TIA develops abruptly and typically do not evolve)
  • Transient global amnesia
  • Psychogenic non epileptic seizure (PNES)
  • Migraine: (+ve symptoms: visual (bright lines), auditory (tinnitus, noises), somatosensory (pain), motor (jerking or repetitive rhythmic movements)
  • Narcolepsy: daytime sleepiness with cataplexy, hypnagogic hallucination and sleep paralysis
  • Movement disorders: tics/ asterixis/choreoathetosis)
  • Hyperventilation: Environmental trigger will be evident
272
Q

Compare syncope vs seizure
Prodrome
Symptoms
Post ictal state

A
273
Q

Compare syncope, seizure, migraine and stroke/tia in LOC, convulsion and paralysis

A
274
Q

What is the pathogenesis of seizure?

A

 Abnormal excessive or synchronous activity in brain leading to epileptiform behavior
* Enhance connectivity
* Enhanced excitatory (e.g. glutamate) transmission
* Failure of inhibitory (e.g. GABA) mechanism
* Changes in intrinsic neuronal properties

275
Q

How to classify seizures?

A
276
Q

How to classify focal seizures?
What are the symptoms depending on location?

A
277
Q

What are the types of generalized seizures?
What are the clinical manifestation?

A
278
Q

What is the postictal SS for seizure?

A
279
Q

What is the history taking for seizures?

A
280
Q

What is the PE for seizure?
What is the biochemical Ix done?

A
281
Q

What are the non basic Ix for seizures?

A
282
Q

What is the principle of antiepileptic drug (AED) treatment?

A

Principle of AED treatment = Monotherapy at the lowest effective dose

AED monotherapy is prefferred initial management approach in epilepsy care since most patients may be successfully managed with the first or second monotherapy utilized with similar efficacy and better patient tolerability compared to polytherapy
Polytherapy may only minimally increase seizure control and can substantially increase AED toxicity, drug interactions, seizure aggravation, noncompliance and cost

283
Q

What drug interactions are there with AEDs?

A
284
Q

What are the indications for antiepileptic drug (AED) initiation?
Wihthdrawal
Precautions

A
285
Q

What are the types of AEDs?
What complications associated with what drug requires genetic testing?

A
286
Q

What can be the surgical treatment option for epilepsy?

A
287
Q

What is the traetment of status epilepticus (Tonic-clonic)?

A
288
Q
A
289
Q

How are the blood tests relevant to suspected epileptic seizures?

A

 To check anti-convulsants levels
 Identify or exclude metabolic causes of epileptic seizures  Identify or exclude metabolic encephalopathy
 Identify metabolic consequences of generalized seizures
* ↑ Muscle enzymes
* Neutrophilia
* Hyperprolactinemia

290
Q

What mistakes are illustrated in the clinical course?

A

 Inappropriate starting of anti-convulsants after one suspected epileptic seizure
 Known narcotic abuser with positive urine test for methadone which makes drug overdose as a possible explanation of loss of consciousness
 Driving is forbidden especially for people working as drivers
 Drug level has not been checked to ensure adequate dosing and compliance prior to add-on therapy

291
Q

Other than common side effects like drowsiness, cerebellar syndrome and drug interactions, what are the specific side-effects of phenytoin, sodium valproate, lamotrigine and topiramate?

A
292
Q

What is the classifciation of meningitis?

A
293
Q

Meningitis vs encephalitis in clinical presentation?

A
294
Q

What are the causes of bacterial meningitis depending ion age and other concomitant conditions?

A
295
Q

What are the causes of viral meningitis?

A
296
Q

What are the causes of subacute meningitis?

A

 Bacterial causes
* Mycobacterium tuberculosis
* Treponema pallidum
 Fungal causes
* Cryptococcus neoformans (Yeasts)
* Coccidioides immitis (Dimorphic fungi)
* Histoplasma capsulatum (Dimorphic fungi)

297
Q

What is cause of malignant meningitis?

A

 Secondary to solid or hematological malignancy
* Solid tumours include breast cancer, lung cancer, GI malignancy and melanoma
* Hematological tumours include acute leukemia and large cells lymphomas
Remarks: Diagnosis of malignant meningitis requires cytological identification of malignant cells within CSF usually accompanied by lymphocytic pleocytosis, high protein and low glucose

298
Q

What is the pathogenesis of bacterial meningitis?

A
299
Q

What is the pathogenesis of viral meningitis?

A
300
Q

What is the pathophysio of increased ICP in meningitis?

A

 Raised ICP in meningitis is primarily due to cerebral edema
* Vasogenic cerebral edema results from increased permeability of BBB (tumor: poor demaraction between the grey and white matter)
* Cytotoxic cerebral edema results from cytotoxic factors produced by bacteria and neutrophils (clear differentiation between grey and white matter)

301
Q

What is the clinical maniestation of meningitis
What symptoms of meningeal irritation
Focal neurological signs
Non specific symptoms of viral meningitis

A
302
Q

What is the history taking for meningitis?

A
303
Q

What is the PE and results meningitis?

A
304
Q

What are the blood tests done for meningitis?

A
  • CBC with DC
  • Electrolyte profile: hypoNa in SIADH
  • Clotting profile
  • Blood culture
  • CSF analysis by lumbar puncture: TCC with differentials + glucose + protein + gram stain + culture with sensitivity testing + enterovirus and HSV PCR + opening pressure
  • CSF smear, culture with sensitivity testing, antigen detection and PCR
    Gram smear and AFB smear: gram +ve diplococci (pneumococcal infection), gram +ve rods and coccobacilli (L.monocytogenes), gram-ve diplococci suggest meningococal infection, gram-ve coccobacilli suggest H.influenzae infection
    Culture: bacterial culture with drug sensitivity testing, viral or fungal culture is indicated if clinical picture suggests viral/fungal meningitis
    PCR: most important for CNS viral infection
  • Blood and urine for viral culture and PCR
  • Throat, rectal swabs for viral culture and PCR
  • Serology: for virus with low seroprevalence rate (arboviruswuc has WNV): virus specific IgM antibodies. Virus with high seroprevalence rate (HSV, VZV, EBV, CMV): less useful for dx of CNS viral infections
305
Q

What is the management of increased ICP?

A
306
Q

What is the medical treatment in adults for meningitis (bacterial, viral crytpococcal, TB) and the duration of treatment

A
307
Q

What is the medical treatment in children for bacterial meningitis and the duration of treatment

A
308
Q

What are the neurologic complications of meningitis?
What about prevention?

A
309
Q

What is the most likely cause of her fallopian tube blockage?
Why did she develop persistent fever after delivery of her baby?
From the CSF examination results, apart from TB meningitis, what other diseases could give a
similar clinical picture?

A

 Tuberculous salpingitis
 Reactivation of TB with development of TB meningitis

 Fungal meningitis
 Partially treated bacterial meningitis

310
Q

What empirical antibiotic regimen was most likely given initially for bacterial meningitis, and what antibiotic change would occur to cover for listeriosis?

A

 IV high dose penicillin G + 3rd generation cephalosporin  Antibiotic change
* High dose ampicillin instead of penicillin G should be changed

311
Q

What are the other complications of TB meningitis and how are they treated?

A

 Hydrocephalus: Shunting
 CN palsy: Corticosteroids
 Brain abscesses: Surgical drainage
 Tuberculoma: Corticosteroids, anti-inflammatory drugs
 Spinal block: Corticosteroids

312
Q

What anti-TB regimen was most likely started for TB meningitis, and how long should she remain on the treatment?

A

 Duration of treatment: 9 – 12 months
 Regimen
* Isoniazid with vitamin B6 (pyridoxine)
* Rifampicin
* Ethambutol
* Pyrazinamide

313
Q

What are the anti TB drugs?
What are there AE?

A
314
Q

Why was dexamethasone given with anti-TB treatment, and under what other circumstances would you add steroids to the treatment?

A

 For anti-inflammatory effects in Medical Research Council Stage II or III disease
 Indicated in
* Lethargy
* Prominent meningeal irritation
* CN palsy
* Convulsion
* Paralysis
* Stupor
* Coma

315
Q

Which of these anti-TB drugs can be safely used in pregnancy with a minimal amount of teratogenicity?

A

 Isoniazid with vitamin B6 (pyridoxine)
 Rifampicin
 Ethambutol

316
Q

What are the contraindications and complications of lumbar puncture?

A

 Contraindications
* Space-occupying lesions (Markedly ↑ ICP)
o Unequal pressures between supra- and infra-tentorial compartments
* Coagulopathy
o Epidural or subdural hematoma
* Spinal block
* Local suppuration
* Local congenital lesion
 Complications
* Headache
* Dry tap
* Brain herniation
* Subdural hematoma
* Aneurysmal subarachnoid hemorrhage

317
Q

What are your differentials for neutrophilic and lymphocytic meningitis?

A
318
Q

What are the general features of encephalitis?

A

 Inflammation of brain parenchyma
 Viral infections of the CNS results in syndrome including aseptic meningitis or encephalitis
 Abnormal cerebral function in encephalitis is the most distinguishing feature between meningitis in which cerebral function remains normal
* Altered mental status
* Personality and behavioral change
* Sensory or motor deficits
* Speech and movement disorders

319
Q

What are the causes of acute encephalitis and chronic encephal

A
320
Q

What are causes of post infectious viral encephalitis?

A

 Common viral infections
* VZV (chickenpox)
* Mumps virus
* Measles virus
* Rubella virus
 Vaccination
* Smallpox
* Rabies virus
* Influenza virus

321
Q

Primary vs post infectious viral encephalitis based on histological examination?

A
322
Q

What is the SS of encephalitis?

A
323
Q

What is the ddx for encephalitis?

A

 Meningitis (bacterial/ viral/ TB/ fungal)
* Complicated with cerebral edema or cerebral venous thrombosis
 Brain tumours (primary/ metastatic)
 Brain abscess
 Syphilis
 Toxic encephalopathy
 Metabolic encephalopathy
* Hypoglycemia
* Electrolyte disturbance

324
Q

What Ix done for encephalitis?

A
325
Q

Treatment and duration for viral encephalitis?

A

 Acyclovir (IV)
* 10 mg/kg Q8h
* For 10 – 14 days

326
Q

What is spread of disease in brain abscess?

A
327
Q

What are the sources of infection in brain abscess?

A
328
Q

What is the pathology of cererbal abscess?

A

 Early stage of lesion (1 – 2 weeks) = Cerebritis
* Acute inflammation with no tissue necrosis
* Poorly demarcated with localized edema
 Late stage of lesion (After 2 weeks)
* Necrosis and liquefaction
* Lesion is surrounded by a fibrous capsule

329
Q

What is SS of brain absce

A

 Fever
 Headache
* Most common presenting complaint
* Onset can be sudden or gradual
* Localized to the side of abscess
* Severe pain which is NOT relieved by aspirin
 Nausea and vomiting
* Associated with increased ICP
 Neck stiffness
 Alteration in mental status
* From lethargy progressing into coma
* Indicates cerebral edema and is a poor prognostic sign
 Focal neurological deficits
* Hemiparesis
* Seizures

330
Q

What is PE of cerebral abscesss?
What is Ix done?

A
331
Q

What is treatment of brain abscess?
What complications?

A
332
Q

What is the etiology of Charcot Marie Tooth disease (also known as hereditary motor sensory neuropathy (HMSN)?
What is the classification?

A

Etiology: CMT1 anfd CMT2 mutation (AD inheritance mostly): located on chromosome 17p
CMT is a group of hereditary of polyneuropathies involving both motor and sensory function

Classification
Type 1: primary demyelinating neuropathy
Type 2: proxmary axonal neuropathy
Type 3: Dejerine-Scottas disease
Type 4: autosomal recessive demyelinating neuorpathy
Type 5: associated with spastic paraplegia
Type 6: maniefsts with neuropathy and optic atrophy
Type 7: manifests with neuorpathy and retinitis pigmentosa

333
Q

What is the clinical presentation of Charcot Mariet tooth disease?

A

Early onset, slowly progressive course. Severity of symptoms depends on subtype, but most ahve normal lifespan

Signs
UL: small hand muscle wasting, claw hands
LL: distal leg muscle wasting (inverted champagne bottle sign
* Pes cavus (hallmark of early onset neuropathy) or pes planus
* Claw toes
* Foot drop high steppage gait +/-ataxis gait
* Romberg test +ve (sensory ataxia)
Motor: LMN signs with length dependent pattern (LL >UL> distal> proximal)
Sensory: gove and stock pattern fo sensory loss, affect DCML but intact ST tract
Secondary OA (Charcot joint)

334
Q

What Ix done for Charcot Mariet Tooth disease?

A

Nerve conduction study: decreased impulse conduction velocity in both sensory and motor nerves
Sural nerve biopsy: hypertrophuic neuropathy (onion bulb appearance from repeated demyelination and remyelination in large nerve fibers

MBBS VI Medicine (92 decks)

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