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MRCS A - Dr Bishoy > 28- neuro Explains > Flashcards

28- neuro Explains Flashcards

1
Q

What is an extradural hematoma?

A

Bleeding into the space between the dura mater and the skull, often resulting from acceleration-deceleration trauma or a blow to the side of the head

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2
Q

Where do the majority of extradural hematomas occur?

A

In the temporal region, where skull fractures cause a rupture of the middle meningeal artery

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3
Q

What are the features of an extradural hematoma?

A

Raised intracranial pressure, and some patients may exhibit a lucid interval

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4
Q

What is a subdural hematoma?

A

Bleeding into the outermost meningeal layer, most commonly around the frontal and parietal lobes

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5
Q

What are the risk factors for subdural hematomas?

A

Old age and alcoholism

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6
Q

How does the onset of symptoms in a subdural hematoma differ from an extradural hematoma?

A

Symptoms in a subdural hematoma have a slower onset compared to an extradural hematoma

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7
Q

What is a subarachnoid hemorrhage?

A

Bleeding that usually occurs spontaneously from a ruptured cerebral aneurysm, but can also be seen in association with other traumatic brain injuries

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8
Q

How does diffuse axonal injury occur?

A

As a result of mechanical shearing during deceleration, causing disruption and tearing of axons

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9
Q

What are the two types of primary brain injury?

A

Focal (contusion/haematoma) and diffuse (diffuse axonal injury)

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10
Q

What are the different types of intra-cranial hematomas?

A

Extradural, subdural, and intracerebral

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11
Q

What happens to cerebral autoregulatory processes following trauma?

A

They are disrupted, making the brain more susceptible to blood flow changes and hypoxia

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11
Q

Where can contusions occur in relation to the impact site?

A

Adjacent to the impact site (coup) or on the opposite side (contre-coup)

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12
Q

What is secondary brain injury?

A

It occurs when cerebral edema, ischemia, infection, tonsillar or tentorial herniation worsens the original injury

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13
Q

What may be required for diffuse cerebral edema?

A

Decompressive craniotomy

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14
Q

What is the Cushings reflex?

A

Hypertension and bradycardia, often occurring late and usually a pre-terminal event

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15
Q

What management options are available for life-threatening rising intracranial pressure?

A

Use of IV mannitol/frusemide while theater is prepared or transfer is arranged

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16
Q

When are exploratory burr holes used in modern practice?

A

When scanning is unavailable and to facilitate creation of a formal craniotomy flap

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17
Q

What is the management for open depressed skull fractures?

A

Formal surgical reduction and debridement

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18
Q

When is ICP monitoring mandatory?

A

In patients with a GCS of 3-8 and an abnormal CT scan

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18
Q

How are closed depressed skull fractures managed?

A

They may be managed non-operatively if there is minimal displacement

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18
Q

What is the most likely cause of hyponatremia in this context?

A

Syndrome of inappropriate ADH secretion

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19
Q

When is ICP monitoring appropriate?

A

In patients with a Glasgow Coma Scale (GCS) of 3-8 and a normal CT scan

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20
Q

What is the minimum cerebral perfusion pressure required in adults?

A

70 mmHg

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20
Q

What is the minimum cerebral perfusion pressure required in children?

A

Between 40 and 70 mmHg

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21
Q

What does unilaterally dilated pupil with sluggish or fixed light response indicate?

A

3rd nerve compression secondary to tentorial herniation

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22
Q

What does bilaterally dilated pupil with sluggish or fixed light response indicate?

A

Poor CNS perfusion

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23
Q

What does bilateral 3rd nerve palsy indicate?

A

Bilateral dilation of the pupils

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24
Q

What does unilaterally dilated or equal pupils with cross reactive (Marcus-Gunn) response indicate?

A

Optic nerve injury

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25
Q

What does bilaterally constricted pupils indicate?

A

It may be difficult to assess, but possible causes include opiates, pontine lesions, and metabolic encephalopathy

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26
Q

What does unilaterally constricted pupil with preserved sympathetic pathway response indicate?

A

Sympathetic pathway disruption

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27
Q

What percentage of subarachnoid hemorrhage cases have normal angiography?

A

Approximately 10%

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27
Q

What imaging is recommended for investigation?

A

CT scan for all cases; lumbar puncture if CT is normal

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27
Q

What is the most common cause of subarachnoid hemorrhage?

A

Intracranial aneurysm (85% of cases)

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28
Q

What is the typical presentation of subarachnoid hemorrhage?

A

> 95% of cases have a thunderclap headache; >15% may have coma

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29
Q

What is the purpose of a CT angiogram in subarachnoid hemorrhage?

A

To look for aneurysms

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30
Q

What is the goal of management for subarachnoid hemorrhage?

A

Supportive treatment, optimizing blood pressure, ventilation if needed

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31
Q

What medication is used to reduce cerebral vasospasm and improve outcomes?

A

Nimodipine

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32
Q

When are untreated patients most likely to experience rebleeding?

A

Within the first 2 weeks

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33
Q

What treatment options are available for aneurysms?

A

Craniotomy and clipping or endovascular coiling

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34
Q

Which treatment option, coiling or surgery, has better outcomes according to available data?

A

Coiling

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35
Q

What is the recommended timeframe for assessing patients with head injuries in the emergency department?

A

Within 15 minutes of arrival

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36
Q

What are the three components of the GCS that should be documented in head injury patients?

A

Eye opening, verbal response, motor response

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37
Q

When should the airway be considered for stabilization in head injury patients?

A

If GCS is less than or equal to 8

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38
Q

When is full spine immobilization indicated in head injury patients?

A

If GCS is less than 15, neck pain/tenderness, paraesthesia extremities, focal neurological deficit, or suspected c-spine injury

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39
Q

What imaging modality is preferred for suspected c-spine injury?

A

CT c-spine

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40
Q

When is an immediate CT head scan recommended (within 1 hour)?

A

If GCS is less than 13 on admission, GCS is less than 15 two hours after admission, suspected open or depressed skull fracture, suspected skull base fracture, focal neurology, vomiting > 1 episode, post-traumatic seizure, coagulopathy (or receiving anticoagulant)

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41
Q

When should a neurosurgeon be contacted in head injury cases?

A

If there is persistent GCS less than or equal to 8, unexplained confusion lasting >4 hours, reduced GCS after admission, progressive neurological signs, incomplete recovery post-seizure, penetrating injury, or cerebrospinal fluid leak

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42
Q

How frequently should GCS be monitored in head injury patients?

A

Every 1/2 hour until GCS reaches 15

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43
Q

What are the two most common types of CNS tumors?

A

Glioma and metastatic disease (60%)

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44
Q

What is the second most common type of CNS tumor?

A

Meningioma (20%)

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45
Q

What percentage of CNS tumors are pituitary lesions?

A

10%

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46
Q

What are the common types of CNS tumors in pediatric practice?

A

Medulloblastomas (neuroectodermal tumors) and astrocytomas

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47
Q

Which areas of the brain may have tumors that reach considerable size before becoming symptomatic?

A

Right temporal and frontal lobes

48
Q

What imaging technique provides the best resolution for diagnosing CNS tumors?

A

MRI scanning

49
Q

Which areas of the brain typically produce early symptoms when tumors are present?

A

Speech and visual areas

50
Q

Which type of tumor can usually be cured with surgery?

A

Meningiomas

51
Q

What is the usual treatment approach for CNS tumors?

A

Surgery, even if complete resection is not possible, to address conditions like rising intracranial pressure and prolong survival and quality of life

52
Q

What does a left homonymous hemianopia indicate?

A

Visual field defect to the left

53
Q

Why is complete resection often not possible for gliomas?

A

Gliomas have a marked propensity to invade normal brain tissue

54
Q

What is the difference between incongruous and congruous defects in visual field defects?

A

Incongruous defects suggest a lesion of the optic tract, while congruous defects suggest a lesion of the optic radiation or occipital cortex

54
Q

Which structure is likely to be affected in a left homonymous hemianopia?

A

Right optic tract

55
Q

What are homonymous quadrantanopias and what mnemonic can be used to remember them?

A

Quadrant visual field defects; PITS (Parietal-Inferior, Temporal-Superior)

56
Q

What does the term “macula sparing” indicate in visual field defects?

A

Lesion of the occipital cortex while sparing the central vision (macula)

57
Q

What are the likely locations of lesions causing homonymous quadrantanopias?

A

Superior quadrant defect suggests a lesion of the temporal lobe, while inferior quadrant defect suggests a lesion of the parietal lobe (PITS mnemonic)

58
Q

What does a bitemporal hemianopia indicate?

A

Visual field defect involving both temporal visual fields

59
Q

What is the likely location of a lesion causing an upper quadrant defect compared to a lower quadrant defect in bitemporal hemianopia?

A

Upper quadrant defect suggests inferior chiasmal compression, commonly due to a pituitary tumor, while lower quadrant defect suggests superior chiasmal compression, commonly due to a craniopharyngioma

60
Q

What is an extradural haematoma?

A

Bleeding between the dura mater and the skull

61
Q

Where do the majority of extradural haematomas occur?

A

Temporal region

61
Q

What is the most common cause of extradural haematomas?

A

Acceleration-deceleration trauma or a blow to the side of the head

62
Q

What is a potential feature of extradural haematomas?

A

Raised intracranial pressure; some patients may exhibit a lucid interval

63
Q

What is a subdural haematoma?

A

Bleeding into the outermost meningeal layer

64
Q

Where do subdural haematomas commonly occur?

A

Around the frontal and parietal lobes

65
Q

What are the risk factors for subdural haematomas?

A

Old age and alcoholism

66
Q

How do the symptoms of subdural haematomas compare to extradural haematomas?

A

Slower onset of symptoms

67
Q

What is an intracerebral haematoma?

A

A hyperdense lesion in the brain

68
Q

How do intracerebral haematomas typically form?

A

Areas of traumatic contusion fuse to become a haematoma

69
Q

What should be considered when large haematomas or those causing mass effect are present?

A

Evacuation of the haematoma

70
Q

What is a subarachnoid haemorrhage?

A

Bleeding that occurs spontaneously, often from a ruptured cerebral aneurysm

71
Q

When does intraventricular haemorrhage commonly occur in adults?

A

In association with severe head injuries

72
Q

What is an intraventricular haemorrhage?

A

Haemorrhage that occurs in the ventricular system of the brain

73
Q

When do the majority of intraventricular haemorrhages occur in neonates?

A

First 72 hours after birth

74
Q

What is a potential cause of neonatal intraventricular haemorrhages?

A

Birth trauma combined with cellular hypoxia and the delicate neonatal CNS

75
Q

What is another name for depressed skull fractures?

A

Signature fractures

76
Q

What causes depressed skull fractures?

A

Focal impact of a moving object on the cranial vault

77
Q

What can high-velocity objects do in depressed skull fractures?

A

Not only disrupt bone, but also drive fracture fragments into the brain

78
Q

What type of defect may blunt objects moving at low velocity produce in the skull?

A

A defect of similar dimensions to the object, known as a signature

79
Q

What parts of the skull can be affected by depressed skull fractures?

A

The outer table alone or both the outer and inner tables

80
Q

When may surgery be required for depressed skull fractures?

A

In cases of open fractures or fractures associated with intracranial hematomas

81
Q

How can uncomplicated fractures without significant cosmetic deformities be managed?

A

Conservatively, without surgery

82
Q

What is the initial imaging modality of choice for depressed skull fractures?

A

CT scanning

83
Q

What is the risk of haematoma requiring removal in adults with concussion and no skull fracture who are conscious and oriented?

A

1 in 6,000

84
Q

What is the risk of haematoma requiring removal in adults with concussion and no skull fracture who are not oriented?

A

1 in 120

85
Q

What is the risk of haematoma requiring removal in adults with a skull fracture who are conscious and oriented?

A

1 in 32

86
Q

What is the risk of haematoma requiring removal in adults with a skull fracture who are not oriented?

A

1 in 4

87
Q

What is Von Hippel-Lindau (VHL) syndrome?

A

An autosomal dominant condition predisposing to neoplasia

88
Q

Where is the abnormality in VHL syndrome located?

A

On the short arm of chromosome 3

89
Q

What are the features associated with VHL syndrome?

A

Cerebellar haemangiomas, retinal haemangiomas with vitreous haemorrhage, renal cysts (premalignant), phaeochromocytoma, extra-renal cysts (epididymal, pancreatic, hepatic), and endolymphatic sac tumours

90
Q

What is the primary intracerebral haemorrhage (PICH) characterized by?

A

Headache, vomiting, and loss of consciousness

91
Q

Which arteries are involved in total anterior circulation infarcts (TACI)?

A

Middle and anterior cerebral arteries

92
Q

What are the common symptoms of TACI?

A

Hemiparesis/hemisensory loss, homonymous hemianopia, and higher cognitive dysfunction (e.g., dysphasia)

93
Q

Which arteries are involved in partial anterior circulation infarcts (PACI)?

A

Smaller arteries of the anterior circulation, such as the upper or lower division of the middle cerebral artery

94
Q

What are the common symptoms of PACI?

A

Higher cognitive dysfunction or a combination of two of the three TACI features

95
Q

Which areas are affected in lacunar infarcts (LACI)?

A

Perforating arteries around the internal capsule, thalamus, and basal ganglia

96
Q

Which arteries are involved in posterior circulation infarcts (POCI)?

A

Vertebrobasilar arteries

96
Q

What are the common symptoms of LACI?

A

Isolated hemiparesis, hemisensory loss, or hemiparesis with limb ataxia

97
Q

What are the common symptoms of POCI?

A

Features of brainstem damage, such as ataxia, disorders of gaze and vision, and cranial nerve lesions

98
Q

What is another name for lateral medullary syndrome?

A

Wallenberg’s syndrome

98
Q

What are the symptoms of lateral medullary syndrome (Wallenberg’s syndrome)?

A

Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy; Contralateral: limb sensory loss

99
Q

What are the common symptoms of a stroke involving the anterior cerebral artery?

A

Contralateral hemiparesis and sensory loss, with lower extremity involvement greater than upper extremity. Disconnection syndrome may also occur.

99
Q

What are the common symptoms of a stroke involving the posterior cerebral artery?

A

Contralateral hemianopia with macular sparing. Disconnection syndrome may also occur.

99
Q

What is Weber’s syndrome characterized by?

A

Ipsilateral III palsy and contralateral weakness

100
Q

What are the common symptoms of a stroke involving the middle cerebral artery?

A

Contralateral hemiparesis and sensory loss, with upper extremity involvement greater than lower extremity. Contralateral hemianopia, aphasia (Wernicke’s), and gaze abnormalities may also be present.

101
Q

What are the common symptoms of a lacunar stroke?

A

Presentation with either isolated hemiparesis, hemisensory loss, or hemiparesis with limb ataxia.

102
Q

What are the common symptoms of a stroke involving the lateral medulla (posterior inferior cerebellar artery)?

A

Ipsilateral symptoms include ataxia, nystagmus, dysphagia, facial numbness, and cranial nerve palsy (e.g., Horner’s syndrome). Contralateral symptoms include limb sensory loss.

103
Q

What are the common symptoms of a pontine stroke?

A

VI nerve involvement leads to horizontal gaze palsy. VII nerve involvement leads to contralateral hemiparesis.

104
Q

What are the features of a third nerve palsy?

A

The eye is deviated ‘down and out’, ptosis (drooping of the eyelid), and the pupil may be dilated (sometimes called a ‘surgical’ third nerve palsy)

105
Q

What are some common causes of third nerve palsy?

A

Diabetes mellitus, vasculitis (e.g., temporal arteritis, SLE), uncal herniation through the tentorium (false localizing sign due to raised ICP), posterior communicating artery aneurysm (pupil dilated), cavernous sinus thrombosis

106
Q

What is Weber’s syndrome?

A

It refers to an ipsilateral third nerve palsy with contralateral hemiplegia, caused by midbrain strokes

107
Q

What are some other possible causes of third nerve palsy?

A

Amyloid, multiple sclerosis

108
Q

Where are the cavernous sinuses located?

A

On the body of the sphenoid bone, running from the superior orbital fissure to the petrous temporal bone

109
Q

What are the medial relations of the cavernous sinuses?

A

Pituitary fossa and sphenoid sinus

110
Q

What are the lateral relations of the cavernous sinuses?

A

Temporal lobe

111
Q

What are the components of the lateral wall of the cavernous sinuses from top to bottom?

A

Oculomotor nerve, trochlear nerve, ophthalmic nerve, and maxillary nerve

112
Q

What are the contents of the cavernous sinuses from medial to lateral?

A

Internal carotid artery (and sympathetic plexus) and abducens nerve

113
Q

What is the blood supply to the cavernous sinuses?

A

Ophthalmic vein, superficial cortical veins, and basilar plexus of veins posteriorly

114
Q

What is the Cushing reflex?

A

The Cushing reflex is a physiological response that occurs when intra cranial pressure (ICP) exceeds mean arterial pressure (MAP), leading to compression of cerebral arterioles and resulting in cerebral ischemia.

114
Q

Where do the cavernous sinuses drain into?

A

The internal jugular vein via the superior and inferior petrosal sinuses

115
Q

What happens during the initial stage of the Cushing reflex?

A

Increases in ICP activate the sympathetic nervous system, causing a stepwise increase in peripheral vascular resistance and hypertension. Cardiac output also increases.

116
Q

What triggers the second stage of the Cushing reflex?

A

The haemodynamic changes detected by aortic arch baroreceptors trigger the activation of the parasympathetic nervous system.

117
Q

What are the parasympathetic effects in the second stage of the Cushing reflex?

A

The parasympathetic effects include a decrease in peripheral vascular resistance and a decrease in cardiac output.

117
Q

Why is the Cushing reflex considered a serious development?

A

The Cushing reflex indicates imminent coning (herniation of the brainstem) or other terminal events if not resolved quickly. It serves as a warning sign of severe neurological compromise.

MRCS A - Dr Bishoy (58 decks)

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