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MHD2 > Block 8 (Neuro) - L9, L10 > Flashcards

Block 8 (Neuro) - L9, L10 Flashcards

1
Q

Where is an epidural abscess located?

A

Space between the bone and the dura

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2
Q

Where is a subdural empyema located?

A

Space between dura and leptomeninges

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3
Q

What is meningitis?

A

Inflammation within the subarachnoid space (between arachnoid and pia mater)

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4
Q

What is encephalitis?

A

Inflammation of brain parenchyma (meningoencephalitis when subarachnoid space is also inflamed)

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5
Q

What is polio, leuko, and panencephalitis?

A

Polioencephalitis - primarily affects the gray matter

Leukoencephalitis - primarily affects the white matter

Panencephalitis - affects both

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6
Q

What is ventriculitis?

A

Inflammation of the ventricles

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7
Q

What are the 5 broad causes of meningitis?

A
  1. Bacterial
  2. Fungal
  3. Amebic and tuberculous
  4. Viral
  5. Non-infectious - chemical (e.g. post-op), meningeal carcinomatosis
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8
Q

What are the most common pathogens causing bacterial meningitis?

A

S. pneumoniae
N. meningitidis
H. influenzae

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9
Q

What pathogens tend to cause acute bacterial meningitis in patients <1 month old?

A
  1. E. coli
  2. Group B strep
  3. L. monocytogenes
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10
Q

What pathogens tend to cause acute bacterial meningitis in patients who are 1 month - 16 years old?

A
  1. N. meningitidis
  2. H. influenzae
  3. S. pneumoniae
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11
Q

What pathogens tend to cause acute bacterial meningitis in adults (>15 y/o) who are immunocompetent?

A
  1. S. pneumoniae

2. N. meningitidis

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12
Q

What pathogens tend to cause acute bacterial meningitis in patients who are immunocompromised (age, diabetes, steroids, alcohol use, etc.)

A
  1. L. monocytogenes

2. Group B strep

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13
Q

What is seen on the gross brain in bacterial meningitis?

A

Pus (thick, creamy exudate composed of protein, bacteria, and neutrophils)

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14
Q

CSF findings - bacteria

Fluid quality?
Cells present?
Protein?
Glucose?
Pressure?
A 
Fluid quality: cloudy
Cells present: PMNs
Protein: very high
Glucose: low (compared to plasma levels)
Pressure: high
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15
Q

What is seen on H&E stain in bacterial meningitis?

A

Subarachnoid space is filled with inflammatory cells (normally empty)

Note - the cortical surface is largely uninvolved

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16
Q

What are the 6 causative agents of chronic meningitis?

A
  1. Tuberculous (M. tuberculosis, rare)
  2. Fungal (Cryptococcus neoformans, Histoplasma capsulatum, Coccidioides immitis)
  3. Parasitic
  4. Syphilis (T. pallidum, rare)
  5. Borreliosis (B. burgdorferi, rare)
  6. Non-infectious (neurosarcoid)
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17
Q

What is seen on histology in CNS tuberculosis prior to development of meningitis?

A

Rich foci (nodules) - small subpial tubercles

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18
Q

What is the clinical presentation of CNS tuberculosis?

A
  1. CN deficits (common)

2. Signs of meningeal irritation (variable)

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19
Q

CSF findings - TB

Fluid quality?
Cells present?
Protein?
Glucose?
Pressure?
A 
Fluid quality: n/a
Cells present: lymphocytes
Protein: moderately high
Glucose: mildly low (compared to plasma levels)
Pressure: n/a
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20
Q

What are the 4 different clinical pathologic patterns seen in CNS TB?

A
  1. Tuberculous meningitis
  2. Tuberculoma
  3. Tuberculous brain abscess
  4. Vertebral osteomyelitis (Pott’s disease)
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21
Q

What is seen on the gross brain in tuberculous meningitis?

A

Thick exudate at the base of the brain

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22
Q

What is seen histologically in CNS TB?

A

Characteristic lesion - necrotizing granuloma

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23
Q

What is a tuberculoma?

A

Space-occupying lesion with a caseous center and granulomatous inflammation; common in patients with miliary TB

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24
Q

What are the 3 clinicopathologic patterns of neurosyphillis?

A
  1. Aseptic meningitis
  2. Meningovascular syphilis
  3. Parenchymal neurosyphilis (general paresis and tabes dorsalis)
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25
Q

What does the CSF show in neurosyphillis?

A

Aseptic meningitis

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26
Q

Discuss the presentation of meningovascular syphilis.

A

Develops months-years after primary infection (earlier in HIV)

Thickened meninges leads to hydrocephalus and CN palsies

Obliterative endarteritis leads to thrombosis and infarction

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27
Q

What is seen morphologically in meningovascular syphillis?

A

Lymphocytic vasculitis

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28
Q

Discuss the presentation of general paresis.

A

Presents 5-25 years after infection

Symptoms: psychosis and dementia

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29
Q

What is seen on pathology in general paresis?

A

Cortical atrophy of frontal and temporal lobes; large number of spirochetes present

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30
Q

Discuss the presentation of tabes dorsalis.

A

Pupillary abnormalities, optic nerve atrophy with declining visual acuity, ataxia, bladder and bowel dysfunction

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31
Q

What is seen on pathology in tabes dorsalis?

A

Posterior spinal roots and columns atrophy; no spirochetes demonstrated

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32
Q

What patients are most likely to get fungal infections of the CNS?

A

Patients who are immunocompromised

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33
Q

The majority of fungal CNS infections are part of systemic infection. List some of the causes.

A
  1. Lung (most common primary site)
  2. Cutaneous mycosis
  3. Sinus or mastoid (zygomycetes)
  4. Infected heart valve
  5. Acquired (iatrogenic)
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34
Q

What are the possible presentations of CNS fungal infections?

A
  1. Meningitis
  2. Encephalitis
  3. Granuloma or abscess
  4. Secondary vasculitis with intracerebral hemorrhage (vascular invasion and thrombosis can lead to infarction; mycotic aneurysm rupture can lead to hemorrhage)
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35
Q

What fungi can cause secondary vasculitis with intracerebral hemorrhage?

A

Aspergillus, Candida, Coccidioides

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36
Q

What are the microscopic findings of fungal infections?

A

Mononuclear infiltrate, variably granulomatous

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37
Q

What are the three special stains for diagnosis of fungal infections?

A
  1. Periodic acid-Schiff (PAS)
  2. GMS
  3. Mucicarmine (Crypto)
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38
Q

What is the gold standard for diagnosis of fungal infections?

A

PCR

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39
Q

What are the 4 major causes of fungal meningitis (hyphal and pseudohypal fungi)?

A
  1. Candida
  2. Aspergillus
  3. Zygomycetes
  4. Fusarium
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40
Q

What are the 3 major causes of fungal meningitis (yeasts)?

A
  1. Histoplasma
  2. Blastomyces
  3. Cryptococcus
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41
Q

What is the most common form of fungal meningitis?

A

Cryptococcus

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42
Q

How is Cryptococcus diagnosed?

A

India Ink stain of CSF

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43
Q

Where is Cryptococcus found and how is it transmitted?

A

Soil and bird feces; inhaled

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44
Q

What is seen on the gross brain in Cryptococcus?

A

Thickened, pale meninges
Clear cystic lesions in the white and deep gray matter
(Swiss cheese effect)

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45
Q

What is seen microscopically in Cryptococcus?

A

Can see oval budding yeasts with a mucoid capsule; inflammation is focal and limited

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46
Q

What are the three major causes of parasitic CNS infections?

A
  1. Cysticercosis
  2. Toxoplasmosis
  3. Amoebiasis (N. fowleri, Entamoeba histolytica, Balamuthia mandrillaris)
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47
Q

What is the most common cerebral parasite?

A

Cysticercosis

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48
Q

Where is Cysticercosis found geographically?

A

SW US and Mexico

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49
Q

How is Cysticercosis transmitted?

A

Consumption of pork tapeworm (T. solium)

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50
Q

What is the most common manifestation of Cysticercosis and what causes the symptoms?

A

Seizures; death of the parasite

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51
Q

What can be seen grossly/on imaging in Cysticercosis?

A

Cysts containing scolexes

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52
Q

How is Toxoplasma gondii transmitted?

A

Consumption of cysts in meat or oocysts inc at feces

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53
Q

Most people are infected after childhood and infection remains silent in Toxoplasmosis - reactivation may follow ___.

A

Immunosuppression

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54
Q

How does toxoplasmosis present in the brain?

A

Abscess leading to seizures and focal neurologic deficits

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55
Q

What can be seen on imaging in toxoplasmosis?

A

Ring enhancing lesion on MRI

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56
Q

What are the TORCH infections?

A

Common infections associated with congenital anomalies

Toxoplasmosis
Others
Rubella
CMV
Herpes virus
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57
Q

What is the classic triad of symptoms seen in congenital toxoplasmosis?

A

Chorioretinitis
Hydrocephalus
Intracranial calcifications

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58
Q

What is seen histologically in Toxoplasmosis?

A

Cyst with bradyzoites, background of necrosis and acute inflammation

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59
Q

What is Naegleria fowleri and what does it cause?

A

Free living amoeba, infects people swimming in freshwater lakes, enters via the cribriform plate

Causes fulminant acute meningoencephalitis (usually fatal)

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60
Q

What do Acanthamoeba and Balamuthia cause?

A

Granulomatous encephalitis with a less fulminant course (still high mortality)

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61
Q

What is the most common cause of viral meningitis?

A

Enteroviruses

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62
Q

CSF findings - viruses

Fluid quality?
Cells present?
Protein?
Glucose?
Pressure?
A 
Fluid quality: clear
Cells present: lymphocytes
Protein: slightly high
Glucose: normal (compared to plasma levels)
Pressure: n/a
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63
Q

What is seen grossly in viral meningitis?

A

Usually nothing; may be hyperemia, congestion, and edema of the brain

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64
Q

What are the microscopic changes seen in viral meningitis?

A

Lymphocytic meningeal infiltrates, perivascular lymphocytic extension along Virchow-Robin spaces

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65
Q

What is encephalitis?

A

Inflammation of the brain parenchyma, diffuse or regional; usually accompanied by meningitis = meningoencephalitis

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66
Q

Most encephalitis is caused by ___.

A

Viruses

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67
Q

What viruses target the meninges?

A
  1. Mumps
  2. Enterovirus
  3. Coxsackie
  4. HIV
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68
Q

What viruses target motor neurons?

A
  1. Polio

2. Enterovirus

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69
Q

What viruses target neurons and glia?

A
  1. Herpes virus
  2. Rabies
  3. Measles
70
Q

What viruses target neurons, glia, and endothelium?

A

CMV (in immunocompromised)

71
Q

What viruses target oligodendroglia?

A

Papovavirus (usually in immunocompromised)

72
Q

What viruses target microglia?

A

HIV

73
Q

What viruses target dorsal root ganglia?

A

HSV, VZV

74
Q

What viruses target the fetal nervous system?

A

Rubella, CMV

75
Q

What viral encephalitis is prevalent in summer/early fall?

A

Arboviruses (WNV)

Also enterovirus, RMSF (non-viral, mimics viral encephalitis)

76
Q

What viral encephalitis is prevalent in fall and winter?

A

LCMV

77
Q

What viral encephalitis is prevalent in winter and spring?

A

Mumps

78
Q

What viral encephalitis is prevalent in any season?

A

HSV

Also EBV, CMV, mycoplasma (non-viral), and leptospira (non-viral)

79
Q

Which type of brain matter is involved more in viral encephalitis?

A

Grey>white

80
Q

What are the microscopic findings in viral encephalitis?

A
  1. Perivascular inflammation
  2. Leptomeningeal inflammation
  3. Microglial clusters (nodules)
  4. Neuronophagia

T-lymphocytes predominate (some PMNs in acute phase)

81
Q

Activated microglial cells are ___-shaped.

A

Comma

82
Q

What transmits WNV?

A

Mosquitos

83
Q

Most WNV infections are asymptomatic; what symptoms are seen when they are present?

A

Polioencephalomyelitis

Parkinsonism

84
Q

What three groups of neurons are targeted by WNV?

A

Anterior horn cells
Nigral neurons
Purkinje cells

85
Q

How is poliovirus transmitted?

A

Fecal-oral, replicates in oropharynx and SI

86
Q

What are the clinical features of polio encephalitis?

A
  1. Asymmetrical paralysis (lower limbs&raquo_space; upper limbs > trunk)
  2. CN palsies (9, 10)
  3. Bulbar disease
  4. Reticular formation (cardiac arrhythmia, sleep apnea, abnormal breathing patterns)
87
Q

Polio encephalitis is restricted to the ___ matter and infects/destroys ___ cells.

A

Grey; anterior horn (LMN)

88
Q

Old lesions caused by polio encephalitis demonstrate what microscopic findings?

A

Loss of motor neurons, anterior nerve root atrophy, and neurogenic atrophy of corresponding muscles

89
Q

What is seen on histology in polio encephalitis?

A

Mixed inflammatory infiltrate, neuronophagia

90
Q

What is the incubation period of rabies?

A

10 days to over 1 year

91
Q

What is seen in neurons of the brainstem, hippocampus, and cerebellum in rabies?

A

Negri bodies (cytoplasmic inclusions)

92
Q

What is the shape of rhabdovirus?

A

Bullet-shaped

93
Q

What type of herpes virus causes herpes encephalitis and how is it transmitted?

A

HSV-1 (usually)

Saliva

94
Q

Herpes encephalitis is an example of a focal encephalitis - where is it found?

A

Medial temporal lobes (edema, hemorrhage, and necrosis)

95
Q

Describe the gross findings of herpes encephalitis.

A

Bilateral, usually asymmetrical hemorrhagic necrosis of the temporal lobes, especially anteriorly and inferiorly, and to a lesser extent, the insulae, cingulate gyri, and thalamus

Usually brain edema

96
Q

What is seen histologically in herpes encephalitis?

A

Owl’s eye intranuclear inclusion

97
Q

Describe the gross findings of chronic herpes encephalitis.

A

“Burnt-out”

Hemorrhagic necrosis will progress to cavitation and atrophy; brain appears shriveled and brown

98
Q

___ is a common opportunistic infection in AIDS and fetal/neonates.

A

CMV

99
Q

What is seen histologically in CMV?

A

Large intracytoplasmic and intranuclear inclusions

100
Q

What is seen grossly in congenital CMV encephalitis?

A

Moderately dilated ventricles and several foci of calcifications in the periventricular region

101
Q

What is seen microscopically in congenital CMV encephalitis?

A

Meningoencephalitis

Inclusions in all cellular elements of the brain, including neurons; most numerous in the periventricular regions

102
Q

What is seen in postnatal congenital CMV infection?

A

Numerous microglial nodules, only occasional cytomegalic cells with inclusions

103
Q

What causes progressive multifocal leukoencephalopathy (ML)?

A

JC virus (genus Polyomavirus)

104
Q

What is seen histologically in PML?

A
  1. Loss of myelin with axonal sparing
  2. Bizarre astrocytes
  3. Oligodendroglial inclusions (ground glass)
105
Q

PML usually affects what patient population?

A

Immunocompromised (reversal of immunosuppression can stop progression of PML)

106
Q

What is seen grossly in PML?

A

Multiple small or larger confluent foci of grey discoloration in the white matter and at the junction of the white matter and cerebral cortex

107
Q

What happens in HIV encephalitis?

A

Widespread microglial nodule encephalitis with multinucleated giant cells with predilection to grey matter

108
Q

What happens in HIV leukoencephalopathy?

A

Subacute onset of cognitive impairment and apathy

Diffuse white matter myelin pallor microglial nodules and multinucleated giant cells

Oligodendrocytes not infected

109
Q

What happens in vacuolar myelopathy?

A

Spastic paraparesis with hyperreflexia and ataxia due to vacuolation of SC white matter

110
Q

What is a brain abscess?

A

Space-occupying focal CNS infection

111
Q

What is the most common cause of brain abscess?

A

Hematogenous spread

Heart (endocarditis, congenital heart defect with shunt)

Lung (bronchiectasis)

Can also be local extension (teeth, ear, frontal sinus), or direct introduction (penetrating head trauma, neurosurgery)

112
Q

Lumbar puncture is not helpful in brain abscess - it may even cause ___.

A

Herniation

113
Q

What is the diagnostic tool of choice for brain abscess?

A

Neuroimaging

114
Q

Definite diagnosis and pathogen identification of brain abscess can be achieved by __.

A

Stereotactic biopsy

115
Q

What is seen on MRI in brain abscess?

A

RIng-enhancing lesion

116
Q

What are 3 other causes of ring-enhancing lesions in the brain?

A
  1. Toxoplasmosis
  2. Glioblastoma
  3. Metastasis
117
Q

What is seen grossly in a brain abscess?

A

Well-circumscribed areas of softening at grey-white junction or in white matter, where collateral circulation is poorest

118
Q

How does an abscess evolve?

A
  1. Early cerebritis (focal encephalitis) - days 1-3
  2. Late cerebritis - day 4-9 (necrotic center surrounded by rim of inflammatory cells, microvascular damage)
  3. Early encapsulation (days 10-13)
  4. Late encapsulation (2+ weeks)
119
Q

What provides anterior (70% of CBF) and posterior (30% of CBF) flow to the brain?

A

Anterior - internal carotid artery

Posterior - vertebral arteries

120
Q

The brain receives ___% of CO and ___% of oxygen consumption - there is no oxygen reserve in the brain.

A

20; 15

121
Q

How long does normal brain function last after cerebral ischemia? When does irreversible damage occur?

A

8-10 seconds;

6-8 minutes

122
Q

What can cause cessation of blood flow to the brain?

A
  1. Hypotension (reduction in perfusion pressure)

2. Small or large vessel occlusion

123
Q

List brain cells most sensitive to ischemia (most to least).

A

Neurons > oligodendrocytes > endothelial cells > astrocytes

124
Q

What is a stroke?

A

Abrupt onset of focal or global neurological symptoms caused by ischemia or hemorrhage

125
Q

What causes 85% of strokes? The other 15%?

A

85% - cerebral ischemia

15% - intracranial hemorrhage

126
Q

What is cerebral ischemia and what are the two major types?

A

Lack of blood flow to the brain (global and focal)

127
Q

What are the two major types of intracranial hemorrhage?

A

Intraparenchymal and subarachnoid

128
Q

What are the major causes of global cerebral ischemia?

A
  1. Low perfusion (atherosclerosis, etc.)
  2. Acute decrease in blood flow (cardiogenic shock, etc.)
  3. Chronic hypoxia (anemia, etc.)
  4. Repeated episodes of hypoglycemia
129
Q

Discuss the magnitude of insult of mild, moderate, and severe global cerebral ischemia.

A

Mild - no permanent damage

Moderate - watershed infarcts and selectively vulnerable regions

Global - diffuse damage

130
Q

Describe the timing and appearance of histologic changes in global cerebral ischemia.

A

Appear 6-12 hours after insult

“Red dead” neurons = cytoplasmic eosinophilic, loss of Nissl substance, dark, pyknotic nuclei

131
Q

What areas are selectively vulnerable to global cerebral ischemia in adults?

A
  1. Pyramidal neurons in cerebral cortex (layers 3 and 5)
  2. Pyramidal neurons of hippocampus (CA1)
  3. Purkinje cells of cerebellum
132
Q

Global cerebral ischemia in the pyramidal neurons in cerebral cortex layers 3 and 5 leads to ___.

A

Laminar necrosis (area of necrosis with preserved superficial cortex)

133
Q

What areas are selectively vulnerable to global cerebral ischemia in infants?

A
  1. Subiculum
  2. Thalamus
  3. Pontine nuclei
134
Q

What is a watershed zone in the brain?

A

Between ACA and MCA circulations

135
Q

What is an ischemic infarction?

A

Regional ischemia resulting in focal neurologic defects lasting >24 hours

136
Q

What are the 3 major causes of ischemic infarct?

A
  1. Thrombotic (in situ or atherosclerotic plaque at bifurcation of internal carotid and MCA)
  2. Embolic (cardioembolic, atheroembolic)
  3. Small vessel disease (HTN, diabetes, vasculitis)
137
Q

Where does a pure sensory stroke occur?

A

Thalamus

138
Q

Where does a pure motor stroke occur?

A

Internal capsule

139
Q

What are the symptoms of a large ischemic stroke in the MCA territory?

A
  1. Contralateral hemiparesis affecting the lower face and upper extremity more than the leg
  2. Similar distribution contralateral hemisensory loss
  3. Contralateral visual field deficits
140
Q

How do embolic and thrombotic ischemic infarcts differ in appearance?

A

Embolic - red

Thrombotic - pale

141
Q

Describe the gross and microscopic appearance of the brain after acute cerebral ischemia.

A

(6-48 hours)
Gross: pale, soft, swollen, indistinct border, blurred grey-white junction

Micro: neuronal ischemia, red dead neurons, pallor/edema after 6-12 hours, infiltration by neutrophils after 1-3 days

142
Q

Describe the gross and microscopic appearance of the brain after subacute cerebral ischemia.

A

(4 days to 3 weeks)

Gross: gelatinous, friable, distinct border, tissue liquefaction

Micro: neutrophils (early), macrophages (4-7 days), vascular proliferation (2-3 weeks)

143
Q

Describe the gross and microscopic appearance of the brain after chronic cerebral ischemia.

A

(>3 weeks)

Gross: cystic, +/- hemosiderin staining, secondary degeneration
Micro: astrocytic gliosis, residual macrophages

144
Q

Describe the gross appearance of an embolic infarction; where is it most common?

A

Usually smaller, centered at gray-white junction; single or multiple, may involve >1 vascular territory; MCA

145
Q

What is a lacunar infarct?

A

Small infarct, up to 1.5 cm, affects areas with end arterial supply (basal ganglia, thalamus, pons, and subcortical white matter), often due to hypertensive small vessel disease

146
Q

What can be seen on histology in a lacunar infarct?

A

Arterial hyalinosis

147
Q

What are the causes of hemorrhagic infarction?

A

Usually embolic, can be secondary (reperfusion)

148
Q

Where can hemorrhage occur intracranially and what are the various causes?

A
  1. Above the arachnoid (epidural and subdural hematomas, typically caused by trauma)
  2. Below the arachnoid (subarachnoid hemorrhages - aneurysms, parenchymal hemorrhages - HTN)
149
Q

What is a subarachnoid hemorrhage?

A

Bleeding into the subarachnoid space

150
Q

What is a common cause of non-traumatic spontaneous subarachnoid hemorrhage?

A

Berry aneurysm

Other: AVM, anticoagulated state

151
Q

What is seen in the CSF due to a subarachnoid hemorrhage?

A

Xanthochromia (yellow hue due to bilirubin)

152
Q

Describe the pathology of a subarachnoid hemorrhage.

A

Gross - “berry-like” thin-walled (no media) outpouchings from arterial branching points; ruptures at the dome

Associated vascular spasm produces global cerebral ischemia

153
Q

Discuss the etiology of saccular (berry) anuerysms.

A

Etiology unclear
Congenital defect in media hypothesized

Genetic component - associated with AD polcystic kidney disease, Ehlers-Danlos, Marfan’s, etc.

Female>Male (2:1)

154
Q

Where are saccular aneurysms most common?

A

Anterior circle of willis (anterior communicating artery)

155
Q

What are common locations of intraparenchymal hypertensive hemorrhage?

A
  1. Putamen
  2. Thalamus
  3. Pons
  4. Cerebellum
156
Q

What is an IPH secondary to rupture of pseudoaneurysms?

A

Charcot-Bouchard (caused by chronic HTN)

157
Q

What are some other causes of IPH?

A

CAA
Vasculitis
Neoplasms

158
Q

What is seen grossly due to a hypertensive hemorrhage?

A

Circumscribed hematoma surrounded by brain tissue, may extend into subarachnoid space or to the ventricles

159
Q

What is seen on microscopy due to a hypertensive hemorrhage?

A

Blood products surrounded by cerebral edema, minimal tissue necrosis, resolution leads to a cystic space with macrophages containing hemosiderin (orange tinge)

160
Q

Primary intraventricular hemorrhages are rare in adults, but common in ___.

A

Premature infants

161
Q

Where do intraventricular hemorrahges occur?

A

Germinal matrix located beneath the ependyma which easily ruptures into the ventricles; instantaneously fatal

162
Q

What are duret hemorrhages?

A

Secondary to compression from herniation of the medial temporal lobe that leads to stretching and ischemia of perforating arterioles; compression can result from a variety of mass lesions (hemorrhages, inflammation, neoplasms)

163
Q

What is an epidural hematoma?

A

Blood between dura and the skull, classically due to fracture of temporal bone with rupture of middle meningeal artery

164
Q

What is seen on CT in an epidural hematoma?

A

Lens-shaped lesion

165
Q

What is an subdural hematoma?

A

Blood underneath the dura covering brain surface, secondary to tearing of bridging veins between dura and arachnoid, usually due to trauma

166
Q

What is seen on CT in an subdural hematoma?

A

Crescent-shaped lesion

167
Q

What are the symptoms of subdural hematoma?

A

Progressive neurologic signs

168
Q

What is herniation?

A

Displacement of the brain due to mass effect or increased intracranial herniation

169
Q

What are the 3 types of herniation?

A
  1. Tonsillar
  2. Subfalcine
  3. Uncal
170
Q

What is a tonsillar herniation?

A

Displacement of cerebellar tonsils into the foramen magnum, causes compression of brain stem and cardiopulmonary arrest

171
Q

What is a subfalcine herniation?

A

Displacement of the cingulate gyrus under falx cerebri, compression of ACA leads to infarction

172
Q

What is an uncal herniation?

A

Displacement of uncus (medial temporal lobe) under tentorium cerebelli, compression of CN III (eye down and out + dilated pupil), compression of PCA - occipital lobe inarct, rupture of paramedian artery (duret hemorrhages)

MHD2 (34 decks)

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