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Neuro > Head/Brain Diseases > Flashcards

Head/Brain Diseases Flashcards

1
Q

What headache does this describe: a person experiencing pain in the muscles of the region of the head and neck.

A

Tension headaches

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2
Q

What headache does this describe: a severe pain in the head, un-associated with the musculature of the head, but associated with vascular disturbances.

A

Migraine headache

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3
Q

What are tension headaches?

A

Primary headaches due to anxiety, stress, and tension. Characterized by tightness, pressure, or pain in the occipital or forehead area (bilateral)

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4
Q

What are migraine headaches?

A

Primary headaches with paroxysmal attacks of headaches (throbbing) often preceded by psychological or visual disturbances. It can be accompanied by nausea, vomiting, drowsiness.

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5
Q

What are the two types of migraine headaches?

A

Classical migraine - associated with a prodromal aura

Common migraine - not associated with a prodromal aura, but can be preceded with vague symptoms

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6
Q

What are the three theories for etiology of migraines?

A
  • vasodilatory theory: extracranial arterial vasodilation during an attack
  • inflammation of the dural membranes
  • altered normal firing of brain neurons
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7
Q

What are cluster headaches?

A

Headaches with repeat occurances over weeks or months with a sudden onset of unilateral pain and short duration. The pain occurs several times per day, mostly during REM sleep.

Other symptoms: red eyes, lacrimation, rhinorrhea, stuffiness of nostrils, etc. (autonomic features)

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8
Q

What are sinus headaches?

A

Headaches that mostly localized to the frontal areas of the head and around the eyes. Bending over exacerbates pain. Often accompanied by nasal congestion and rhinorrhea.

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9
Q

How are tension headaches treated?

A

counseling, massage, heat application, rest, relaxation

non-narcotic analgesics, anxiolytic drugs

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10
Q

What are preventive treatments for migraines?

A

propranolol - decreases frequency and severity

methysergide - serotonin antagonist

amitriptyline

calcium channel blockers

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11
Q

What are non-pharmacologic treatments for migraine headaches?

A

exercise, relaxation, avoiding dietary triggers

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12
Q

What are the abortive treatments for migraines?

A
  • salicylates and acetaminophen (mild cases)
  • triptans
  • ergotamine
  • narcotic analgesics
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13
Q

What is the treatment for cluster headaches?

A

methysergide - prophylactic serotonin antagonist

can also use propranolol, amitriptyline, calcium channel blockers, and corticosteroids

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14
Q

What is the mechanism of ergotamine?

A

Alpha-adrenoreceptor antagonist that directly constricts vascular smooth muscle

it asks as a serotonin antagonist

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15
Q

What are symptoms of ergot poisoning?

A

vomiting, diarrhea, unquenchable thirst, tingling/itching/coldness of skin, rapid and weak pulse, confusion and unconsciousness, abortion in pregnant women

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16
Q

What is the mechanism of methysergide?

A

Serotonin antagonist that acts as a weak adrenolytic agent, vasoconstrictor, and uterine constrictor

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17
Q

What are the symptoms of methysergide toxicity?

A

retroperitoneal fibrosis, fibrous tissue adhesions on kidney/lung/heart/aorta/viscera

CNS effects (drowsiness, unsteadiness, weakness, etc)

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18
Q

What is the mechanism of -triptan drugs?

A

They activate 5-HT receptors in the nerve to reduce the release of 5-HT, leading to vasoconstriction of cranial blood vessels

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19
Q

What are oligodendrocytes?

A

Myelinating cells of the CNS, have perfectly round and dark nuclei with perinuclear halo

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20
Q

What do astrocytes look like?

A

oblong nuclei with fine chromatin and cytoplasm that blends in with background parenchyma

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21
Q

What is the appearance of microglia?

A

in “activated states” –> have thin, elongated, hyperchromatic nuclei

these are the resident macrophages of CNS

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22
Q

What is the appearance of the ependyma?

A

single layer of cuboidal/columnar ciliated cells that line the ventricular system and form part of the brain-CSF barrier

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23
Q

What are the effects and morphological features of acute neuronal injury?

A

occurs 12 hours after an acute, sustained neuronal injury and results in neuronal cell death

morphologic features: cell shrinkage, intensely eosinophilic (“red dead”) cytoplasm, pyknotic nucleus, loss of nucleolus

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24
Q

What are the effects and morphologic features of subacute/chronic neuronal injury?

A

long-standing neuronal injury as part of progressive diseases

morphologic: progressive cell loss of functinoally associated groups, leads to hyperplasia and hypertrophy of astrocytes

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25
Q

What are the morphologic features associated with axonal injury?

A

rounding up and ballooning of cell body, dispersion of Nissl substance peripherally, and peripheral displacement of nucleus with enlarged nucleolus

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26
Q

What are some examples of neuronal inclusions? Proteinopathies?

A

Neuronal inclusions - cytoplasmic or intranuclear

Proteinopathies - aggregates of misfolded proteins that accumulate in neurodegenerative disease (ex. lewy bodies in parkinsons)

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27
Q

What changes and morphologies are associated with astrocyte gliosis?

A

hypertrophy and hyperplasia of astrocytes in response to CNS injury

morphologic: enlarged, eccentric nuclei with abundant, eccentric, eosinophilic cytoplasm

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28
Q

What are alzheimer type 2 astrocytes?

A

astrocyte changes that occur with long-standing metabolic disorders (not Alzheimer’s disease)

morphologic features: enlarged nucleus, light chromatin, prominent nuclear membrane/nucleolus

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29
Q

What are rosenthal fibers? When do they occur?

A

morphologic features: thick and elongated, brightly eosinophilic, corkscrew-shaped structures in astrocytic processes

diseases: long-standing gliosis, slow growing tumors, some metabolic disorders of white matter

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30
Q

What is corpora amylacea?

A

Changes seen inaging or areas of long-standing injury, thought to represent degenerative changes in astrocytes

morphologic features: round, basophilic, concentrically lamellated structures prominent in areas of astrocytic end processes, may be calcified

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31
Q

What are the responses of microglia to injury?

A
  • elongated shapes (“rod cells”)
  • increased numbers
  • microglial nodules (aggregates around areas of necrosis)
  • aggregates around dying neurons (neuronophagia, prominant in polio and ALS)
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32
Q

What conditions lead to oligodendrocyte injury?

A

demyelinating disorders and leukodystrophies

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33
Q

What diseases are associated with oligodendrocyte inclusions?

A

progressive multifocal laukoencephalopathy, neurodegenerative diseases

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34
Q

What are ependymal granulations?

A

disruption of ependymal lining with proliferation of subependymal astrocytes and formation of pinched of ependymal canals

occurs as a nonspecific reaction to injury

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35
Q

What is vasogenic edema?

A

cerebral edema due to increased extracellular fluid which occurs when the normal BBB is disrupted, resulting in increased vascular permeability that can be localized or generalized

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36
Q

What are the macroscopic characteristics of cerebral edema?

A

flattening of gyri, narrowing of sulci, and compression of the ventricular system

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37
Q

What is cytotoxic edema?

A

cerebral edema due to increased intracellular fluid secondary to cell injury, leads to inability to maintain normal membrane ionic gradients

common etiologies: hypoxic-ischemic injury, metabolic derangements

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38
Q

What is noncommunicating (obstructive) hydrocephalus?

A

increased CSF volume in the ventricular system caused by blockage in the ventricles preventing CSF from reaching subarachnoid space

leads to enlargement of the ventricular system proximal to blockage

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39
Q

What is communicating hydrocephalus?

A

hydrocephalus where CSF in ventricles can communicate freely with the subarachnoid space but leads to enlargement of the entire ventricular system (due to increased production of CSF, scarring of arachnoid granulations, etc)

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40
Q

What are the effects of increased intracranial pressure?

A

decreased perfusion (which can further raise ICP), displacement of tissue, herniations

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41
Q

What is a subfalcine (cingulate) herniation?

A

herniation of the cingulate gyrus under the falx, can compress the ipsilateral anterior cerebral artery

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42
Q

What is a transtentorial (uncal) herniation?

A

Herniation of the uncus/medial temporal lobe through the free margin of the tentorium

can lead to compression of CN III, ipsilateral posterior cerebral artery, and ipsilateral cerebral peduncle

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43
Q

What are duret hemorrhages?

A

linear midline and paramedian hemorrhages that result from torn perforating vessels of the midbrain and pons

occurs with progression of the transtentorial herniation

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44
Q

What is a cerebellar tonsillar herniation?

A

life-threatening herniation of the cerebral tonsils through the foramen magnum with compression of vital cardiac/respiratory centers in the medulla

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45
Q

What do perforating arteries supply?

A

they branch off the circle of Willis and supply the deep gray and white matter structures (basal ganglia, diencephalon, and internal capsule)

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46
Q

What are causes of focal cerebral ischemia?

A

embolism from a distant source, in situ thrombosis (often due to atherosclerosis), inflammatory processes of vessels, pro-thrombotic conditions

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47
Q

What is global cerebral ischemia?

A

a condition also called diffuse hypoxic-ischemic encephalopathy, caused by generalized reduction in cerebral blood flow that may cause irreversible damage to CNS tissue

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48
Q

Which neurons are most susceptible to injury in global cerebral ischemia?

A
  • pyramidal neurons in CA1 region of hippocampus
  • cerebellar Purkinje cells
  • pyramidal neurons in neocortical layers 3 and 5 (watershed areas)
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49
Q

What are the prolonged effects of global cerebral ischemia?

A

widespread neuronal death, liquefactive necrosis

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50
Q

What are the general characteristics of nonhemorrhagic infarcts?

A

nearly identical to focal and global ischemia

initially nonhemorrhagic infarcts can undergo hemorrhagic transformation

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51
Q

What are the macroscopic findings of acute nonhemorrhagic infarcts?

A

no abnormalities within the first 8 hours, after 8 hours can lead to subtle blurring of gray-white junctions

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52
Q

What are the macroscopic findings of subacute nonhemorrhagic infarcts?

A

prominent softening, blurring of gray-white junction, tissue becomes more gelatinous and friable

occurs between 2-10 days

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53
Q

What are the macroscopic findings of a resolving nonhemorrhagic infarct?

A

repair process begins with liquefactive necrosis that is gradually removed and leaves to progressive cavitation

occurs after 10+ days to several months

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54
Q

What are the macroscopic findings of a remote nonhemorrhagic infarct?

A

The repair process is complete and left with CSF-filled cystic cavity

occurs after several months

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55
Q

What are the microscopic findings of an acute nonhemorrhagic infarct?

A

no changes within 12 hours, “red dead” neurons appear at 12 hours and can persist for days, influx of neutrophils

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56
Q

What are the microscopic findings of a subacute nonhemorrhagic infarct?

A

macrophages (seen at 48 hours), reactive astrocytes and capillary proliferations appear at the periphery

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57
Q

What are the microscopic findings of a resolving nonhemorrhagic infarct?

A

repair process begins as liquefactive necrosis proceeds with removal of necrotic tissue by macrophages

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58
Q

What are the microscopic findings of a remote nonhemorrhagic infarct?

A

complete repair process, some macrophages remain

left with cystic cavity and rim of reactive astrocytes

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59
Q

What are lacunar infarcts?

A

small perivascular, ischemic, cavitary infarcts that are seen in hypertension

most often involve the putamen, globus pallidus, thalamus, internal capsule, deep white matter, caudate nucleus, and pons

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60
Q

What is vascular dimentia?

A

neurologic decline as a result of multiple, bilater gray and white matter infarcts that can mimic other neurodegenerative diseases

often due to multifocal vascular disease of different types

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61
Q

What are ganglionic hemorrhages?

A

deep gray and white matter hemorrhages, most often in the putamen/thalamus/pons/cerebellum, caused by hypertension

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62
Q

What are the macroscopic findings of ganglionic hemorrhages?

A

acute - central core of clotted blood with compression of surrounding parenchyma

subacute - resorption of hematoma, friable and gelatinous surrounding tissue

resolving - liquefactive necrosis and progressive cavitation and gliosis

remote - cavitary lesion with brown rim

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63
Q

What are the microscopic findings of ganglionic hemorrhages?

A

acute - central acute hemorrhage and “red dead” neurons

subacute - influx of hemosiderin and lipid-laden macrophages

resolving - removal of necrotic tissue by macrophages with progressive cavitation

remote - cavitary lesions lined by gliosis and hemosiderin-laden macrophages

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64
Q

What are lobar hemorrhages? Microscopic features?

A

intraparenchymal hemorrhages involving cerebral hemispheres, most often caused by cerebral amyloid angiopathy

microscopic features: rigid leptomeningeal and intracortical vessels, vessel walls with dense/glassy pink material, positive stain for beta-amyloid

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65
Q

What are secondary hemorrhagic infarcts?

A

hemorrhagic transformation of an initially non-hemorrhagic ischemic infarct

leads to petechial hemorrhages

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66
Q

What is the most common non-traumatic cause of subarachnoid hemorrhage?

A

saccular (berry) aneurysm

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67
Q

Where do saccular aneurysms most commonly form?

A

arterial branch points in the anterior circulation

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68
Q

What are the macroscopic and microscopic findings of saccular aneurysms?

A

macroscopic: wide or narrow-necked thin walled outpouching, usually at an arterial branch point
microscopic: saccular wall that lacks internal elastic lamina and smooth muscle media (instead made of thickened intima and adventitia)

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69
Q

What are the macroscopic and microscopic findings of vascular malformations?

A

macroscopic: mass of irregular, tortuous, “worm-like” vessels in the subarachnoid and/or intraparenchymal
microscopic: large caliber vessels involving the subarachnoid space and/or brain parenchyma

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70
Q

Cell injury in the central nervous system is characterized by all the following EXCEPT:

a) red dead neurons
b) gliosis
c) microglial nodules
d) ciliated columnar cells lining the ventricles

A

d) ciliated columnar cells lining the ventricles

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71
Q

The following areas are most sensitive to hypoxic-ischemic injury EXCEPT:

a) caudate nucleus
b) CA1 region of hippocampus
c) cerebellar Purkinje cells
d) watershed cortical areas

A

a) caudate nucleus

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72
Q

All of the following are true about cerebral infarcts EXCEPT:

a) remote infarcts are usually cystic
b) remote infarcts can be dated based solely on histopathology
c) macrophages are a prominent feature of subacute infarcts
d) lacunar infarcts originate from arteriosclerosis of deep perforating arterial vessels

A

b) remote infarcts can be dated based solely on histopathology

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73
Q

What is this?

A

Red dead neurons

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74
Q

What is this?

A

axonal reaction with central chromatolysis

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75
Q
A

C) 12 hours

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76
Q
A

B) hypertension

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77
Q
A

D) 2 years

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78
Q

All pathways using glutamate are ________; all pathways using GABA are ________.

A

excitatory; inhibitory

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79
Q

What is the mainr eceiving area of the basal ganglia?

A

Striatum

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80
Q

The cerebral cortex sends _________ __________ projections to the striatum in a somatotopic fashion.

A

excitatory glutamatergic

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81
Q

In the basal ganglia, somatosensory and motor areas project to the __________ and association cortex to the _________.

A

putamen; caudate

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82
Q

What is the primary role of the substantia nigra?

A

Regulating dopamine production to modulate the direct and indirect pathways

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83
Q

What is the path of the indirect pathway of the basal ganglia?

A

D2 efferents (striatum) project to external globus pallidus (inhibitory) –> projects to subthalamic nucleus (eGP inhibits STN, so STN is uninhibited since eGP activity is inhibited) –> projects to GPi and SNr (STN excites them) –> projects to venterolateral and ventral anterior nuclei of the thalamus then the cerebral cortex (inhibits them)

disinhibition of STN ultimately leads to inhibition of the motor cortex and dampening of motion

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84
Q

What is the path of the direct pathway of the basal ganglia?

A

D1 efferents project directly onto the GPi/SNr (inhibits them) –> projects to the VL nucleus of the thalamus (uninhibits it, leading to motion)

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85
Q

What is the effect of a lesion of the substantia nigra pars compacta?

A

disruption of the pathway –> results in loss of dopamine, loss of inhibitory effects on striatum –> increased inhibition of the GPe, disinhibition of the STN, and therefore GPi

excitation of the GPi is also enhanced by lack of inhibition via the direct pathway

ultimate effect: slow movement, lack of movement, parkinsonism

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86
Q

What changes in the basal ganglia pathway lead to dyskinesias and hyperkinetic movements?

A

STN and GPi become excessively inhibited and do not suppress unwanted movements

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87
Q

What are the general criteria for parkinsonism?

A

brady kinesia + one other feature (rigidity and/or tremor)

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88
Q

How is parkinson’s disease definitively diagnosed?

A

pathological confirmation of the presence of degeneration of SNc and other brain stem pigmented nuclei, and the presence of Lewy bodies

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89
Q

What are Lewy bodies?

A

histopathological hallmarks of parkinson’s disease

intracytoplasmic inclusion bodies found in SNc, locus ceruleus, dorsal nucleus of vagus, pigmented nuclei, and cerebral cortex

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90
Q

How is parkinson’s disease diagnosed clinically?

A

Clinical evaluation of symptoms with some imaging (MRI, PET and SPECT tracers, etc)

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91
Q

What are some other diseases that should be considered in the parkinson’s disease differential?

A

progressive supranuclear palsy

multiple system atrophy

dementia with lewy bodies

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92
Q

What is the treatment for parkinsonism?

A

Levodopa - a precursor to dopamine that is capable of crossing the blood brain barrier

Also treated with dopamine agonists, COMT-inhibitors, MAO-B inhibitors, amantadine, and deep brain stimulation

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93
Q

How is levodopa converted to dopamine?

A

it is converted by aminoacid decarboxylase

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94
Q

What is the role of MAO-B inhibitors in treatment of parkinson’s disease?

A

MAO-B inhibitors block reuptake of dopamine and enhance dopamine’s effect in the synapse

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95
Q

What are the long term effects of levodopa treatment?

A

can lead to motor complications and dyskinesias

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96
Q

What are the most common clinical features of parkinsonism?

A

bradykinesia (required)

tremor, rigidity, postural instability, premotor symptoms (hyposomia, constipation, etc) and nonmotor symptoms (anxiety, cognitive impairment, etc)

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97
Q

How is the diagnosis of Parkinson’s disease made?

A

Clinically - based on history, exam, and sometimes imaging to rule out other conditions that can mimic PD

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98
Q

What are the diagnostic criteria for multisystem atrophy?

A

autonomic failure, levodopa resistant parkinsonism, and cerebellar dysfunction

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99
Q

What is the “hot cross bun” sign?

A

cruciform hyperintensity in an atrophied pons in multisystem atrophy due to selective loss of myelinated transverse pontocerebellar fibers

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100
Q

What are the characteristic features of progressive supranuclear palsy?

A

downward gaze abnormalities, postural instability, unexplained falls, bradykinesia and rigidity (symmetrical), non-motor symptoms, pseudobulbar palsy

definite diagnosis: Tau neurofibrillay tangles/straight filaments on histopathology

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101
Q

What are the core clinical features of cortico-basal syndrome?

A

cortical dysfunction (dementia, asymmetric apraxia, alien limb phenomena, cortical sensory loss, visual neglect)

extrapyramidal dysfunction (asymmetric parkinsonism, action tremor, focal limb dystonia, myoclonus)

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102
Q

What is the “triad” associated with dementia with lewy bodies?

A

visual hallucinations, fluctuating cognition, parkinsonism

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103
Q

Which PD patients are ideal deep brain stimulation candidates?

A

tremor is a significant symptom

unpredictable off periods

responds well to levodopa

good surgical risk

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104
Q

What is a tremor?

A

involuntary, rhythmic, oscillatory, sinusoidal movement about a joint produced by contractions of reciprocally innervated antagonist muscles

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105
Q

Describe benign essential tremor.

A
  • action-kinetic, postural, during voluntary movement, rarely at rest
  • worse with anxiety, fatigue, temperture extremes, older age
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106
Q

What is chorea?

A

excessive spontaneous movements from a flow of muscle contractions that are “dance-like”: irregularly timed, randomly distributed, abrupt, and semi-directed

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107
Q

What is the treatment of chorea?

A

neuroleptics (dopamine receptor blockers)

dopamine depeleting agents

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108
Q

What is dystonia?

A

sustained, but not fixed muscle contraction that can cause twisting or repetitive movements and abnormal postures

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109
Q

What are tics?

A

sudden, brief, intermittent movements or utterances that are briefly suppressible and usually associated with an urge for the action

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110
Q

What is myoclonus?

A

brief, “lightening”-like muscle jerks

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111
Q

What is bacterial meningitis?

A

An acute purulent infection within the subarachnoid space, associated with increased intracranial pressure, decreased consciousness, seizures, and stroke

112
Q

What are the most common organisms responsible for bacterial meningitis?

A

strep pneumonia, neisseria meningitidis, group B strep, listeria monocytogenes

113
Q

What is the most common pathogenesis of CNS infection?

A

hematogenous transmission

114
Q

What are the three main types of transmission of CNS infections?

A

hematogenous transmission

contiguous spread

neuronal transmission

115
Q

What is the classic clinical presentation of meningitis?

A

fever, headache, meningismus (nuchal rigidity or stiff neck)

progresses to cerebral dysfunction

can also include nasuea, vomiting, shaking chills, seizures, cranial nerve palsies (rarely)

116
Q

What are signs of increased intracranial pressure?

A

CN III palsy, uni- or bilateral pupillary dilatation, papilledema, Cushing’s reflex, decerebrate posturing, coma

117
Q

What are the CSF findings of bacterial meningitis?

A

decreased CSF glucose (due to increased glycolysis by neutrophils)

increased CSF protein (altered BBB permeability)

CSF culture and gram stain

118
Q

What is the treatment for bacterial meningitis?

A

empiric antibiotic regimen (ceftriaxone + vancomycin + ampicillin)

corticosteroids

119
Q

What are the complications of bacterial meningitis?

A

focal neurologic deficits, cognitive impairment, seizure disorder, hydrocephalus (communicating and obstructive)

120
Q
A
121
Q

What is aseptic meningitis?

A

any meningitis that does not have a clear cause after initial evaluation with stains and cultures of CSF

122
Q

What are causes of subacute/chronic meningitis?

A

mycobacterium tuberculosis, cryptococcus neoformans, syphilis, systemic diseases and neoplasms

123
Q

What is encephalitis?

A

inflammation of the brain parenchyma

124
Q

What is the pathogenesis of encephalitis?

A

mostly hematogenous spread, but can be due to neuronal transmission (ex. reactivation of latent HSV 1)

125
Q

What is the clinical presentation of encephalitis?

A

fever, headache, altered consciousness, focal/multifocal neurological signs, seizures

126
Q

What is the most common cause of focal encephalitis? What are the associated symptoms?

A

HSV-1 encephalitis

fever, headache, altered consciousness, hemiparesis, seizure activity, temporal lobe dysfunction

127
Q

What is the pathogenesis of brain abscesses?

A

continuous spread from untreated frontal sinusitis or other nearby source

128
Q

What are the clinical features of brain abscesses?

A

classic triad: fever, headache, focal neurologic deficit

frontal lesions –> drowsiness, inattention, deteriorated mental function

temporal lesions –> aphasia

cerebellar lesions –> nystagmus, ataxia, vomiting, and dysmetria

129
Q

How are brain abscesses diagnosed?

A

CT, but MRI is better

LP contraindicated

130
Q

What is the treatment for a brain abscess?

A

drainage - percutaneous or surgical

prolonged antibiotics

131
Q

hat is a spinal epidural abscess?

A

infection that spreads in the spinal epidural space (more likely in spine than cranium because the dura is less tightly adhered)

132
Q

What is neurocysticercosis?

A

disease caused by pork tapeworm in humans

can present as an intestinal infection or a neurologic infection (with seizures, hydrocephalus, and inflammation/scarring)

133
Q

What is ciguatera fish poisoning?

A

foodbourne illness caused by eating reef fish contaminated with toxins

symptoms: diarrhea, vomiting, numbness, itchiness, temperature sensitivity, neurologic symptoms

134
Q

An 18 year-old woman presents with abrupt onset of fever, chills, severe headache, and stiff neck. Examination of her cerebrospinal fluid shows an elevated opening pressure; 33 RBCs, 1,200 WBCs, protein 388, and glucose 17. Gram stain of the fluid shows rare gram-negative diplococci. She is a college freshman and lives in a dorm with three roommates. Can treatment be safely narrowed based on CSF gram stain results? How did she acquire infection? Is it vaccine-preventable? How would you counsel her roomates and college?

A

consistent with neisseria meningitidis - therapy narrowed to ceftriaxone alone

acquired person-to-person via respiratory droplets

it is vaccine-preventable

can be passed to close contacts

broader college population should be vaccinated

135
Q

A 72 y.o. man presents with fever, headaches, and dsyphagia. A stat CT scan of the brain (without contrast infusion) is unremarkable. A lumbar puncture is performed and shows 3 RBCs, 48 WBCs, protein 43, and glucose 57. Is further testing necessary? What treatment is recommended? Can he be safely discharged?

A

CSF suggests mild asceptic/viral meningitis, but focal neurologic deficits suggest focal encephalitis

differential includes HSV-1 encephalitis

further testing necessary, empiric treatment indicated

not safe to discharge

136
Q

What are gliomas? What are the two main histologic subgroups?

A

primary CNS tumors from neuroepithelial tissue

subgroups: astrocytoma and oligodendroglioma

137
Q

What are the WHO grades for tumors?

A

Graded I-IV based on severity

I and II = low grade

III/IV = high grades

138
Q

What are the four grades of astrocytic tumors?

A

Grade I = pilocytic astrocytoma

Grade II = astrocytoma

Grade III = anaplastic astrocytoma

Grade IV = glioblastoma multiforme

139
Q

What are the types/grades of oligodendroglial tumors?

A

grade II = oligodendroglioma

grade III = anaplastic oligodendroglioma

140
Q

What are the types/grades of ependymal tumors?

A

Grade II = ependymoma

Grade III = anaplastic ependymoma

141
Q

What staining can identify astrocytic tumors?

A

glial fibrillary acidic protein

142
Q

What is the prognosis of glioblastoma multiforme?

A

very poor - most common malignant primary brain tumor

143
Q

What is the gross and microscopic appearance of glioblastoma multiforme?

A

gross: necrotic, yellowish mass that diffusely infiltrates the normal brain
microscopic: increased cellularity, pleomorphism, atypia, mitoses, pseudo-palisading necrosis, and microvascular proliferation

144
Q

What is the treatment for glioblastoma multiforme?

A

neurosurgery to improve patient function and improve effectiveness of radiotherapy and chemotherapy

other targeted therapy (ex. anti-VEGF antibody)

145
Q

What are oligodendrogliomas?

A

tumors of glial cells that are usually supratentorial and arise in the frontal lobes and are often heavily calcified

146
Q

What are the gross and microscopic findings of oligodendroglioma?

A

gross: similar to astrocytomas but calcified
microscopic: fried egg appearance (cleared cytoplasm), distinct cell borders, and small bland hyperchromatic nuclei

chicken wire branching vessels

147
Q

What are the main markers for oligodendrogliomas?

A

loss of heterozygosity for chromosomes 1p and 19q (1p19q codeletion)

148
Q

What is the cause of death associated with oligodendrogliomas in most patients?

A

transformation into anaplastic oligodendrogliomas

149
Q

What are meningiomas?

A

slow-growing often benign tumors that arise from the meningothelial cap cells of the meninges

150
Q

What are the risk factors for meningiomas?

A

genetic predisposition (neurofibromatosis type 2) and prior exposure to ionizing radiation

151
Q

What is the gross morphology of meningiomas?

A

lobulated tumors with a rubbery consistency

they separate easily from brain tissue (but can invade sinuses and encase arteries)

152
Q

What are the most common presenting symptoms associated with meningiomas?

A

focal seizures, neurologic deficits, and other location-specific signs

153
Q

What type of tumor is this most consistent with?

A

meningioma

154
Q

What is the treatment for meningiomas?

A

monitoring if small or asymptomatic/medically controlled

surgery (can be curative if completely resected)

unresectable tumors get radiation therapy

155
Q

What is a schwannoma?

A

A tumor that arises from the nerve sheath (can occur anywhere in the body, but most common in the vestibular part of the CN VIII)

156
Q

What is the main risk factor for schwannoma?

A

unilateral = sporadic

bilateral = almost always neurofibromatosis type 2 (mutation in the merlin gene)

157
Q

What is the clinical presentation of vestibular schwannomas?

A

gradual, unilateral hearing loss sometimes preceded or accompanied by tinnitus and a vague feeling of dizziness/unsteadiness while walking

can also present with hemifacial spasm and facial numbness

158
Q

What are the physical exam findings and imaging findings associated with schwannomas?

A

exam: ipsilateral decreased facial sensation, cerebellar ataxia, nystagmus, increased ICP
imaging: on MRI, characteristically isointense with nerve on T1-weight, isointense with CSF on T2- weight (harder to see), contrast intensely

159
Q

What is the treatment for vestibular schwannomas?

A

surgical resection and radiosurgery to cure tumor and preserve function

160
Q

What are pituitary adenomas?

A

tumors of pituitary tissue that alters endocrine function (either directly or by compressing normal tissue)

as it grows, it can cause headaches and compression of cranial nerves

161
Q

How are pituitary tumors diagnosed?

A

Imaging: contrast enhanced MRI (hypointense on T1) and calcification seen on CT

Blood: hormone levels measured in the blood

162
Q

How are pituitary adenomas treated?

A

Surgically, may also be treated with suppression of hormone hypersecretion

163
Q

What is a primary central nervous system lymphoma?

A

a non-Hodgkin’s lymphoma that arises within the CNS, predominantly a large B cell tumor with a multifocal angiocentric pattern of growth

immunodeficiency is a risk factor

164
Q

What are the imaging findings of a primary central nervous system lymphoma?

A

usually involves the frontal lobes, corpus callosum, and deep periventricular brain structures

MRI: hypointense on T1 and hypo/isointense on T2, usually homogenous enhancement with IV contrast

165
Q

What are the symptoms of primary central nervous system lymphoma?

A

cognitive impairment, behavioral changes

seizures

headache, hemiparesis/hemisensory loss

note: do not have classic lymphoma B cell symptoms like fever, night sweats, weight loss, etc.

166
Q

How are primary central nervous system lymphomas diagnosed?

A

requires histology for diagnosis (imaging can help, but not definitive)

167
Q

What is the treatment for primary CNS lymphoma?

A

radiotherapy and chemotherapy (sensitive to both) on the whole brain + systemic methotrexate at a high dose

NOT corticosteroids - can make them undetectable for a bit, but then they come back

168
Q

What are the risks associated with therapy for primary CNS lymphoma?

A

neurotoxicity that can lead to dementia, ataxia, and urinary incontinence

169
Q

What are medulloblastomas? Where do they usually localize?

A

malignant childhood tumor

normally localized to the vermis of the cerebellum, but can seed in the leptomeninges and cause widespread metastases

170
Q

What are the histological features of medulloblastoma?

A

densely packed cells with round, oval nuclei surrounded by scanty cytoplasm

homer wright rosettes found 40% of the time

171
Q

What are the most common presenting symptoms of medulloblastoma?

A

presents in children with headache and vomiting (often projectile and without preceding nausea)

symptoms often only present in the morning after first waking up

also includes gait ataxia (vermis controls balance) –> children appear “drunk”

also have other cerebellar abnormalities on exam

hydrocephalus is often present at diagnosis

172
Q

What imaging findings are associated with medulloblastoma? Histology findings?

A

imaging: intense, homogenously enhancing mass in the vermis without evidence of cyst formation or necrosis
histology: small, round undifferentiated cells with mild/moderate nuclear pleomorphism

173
Q

How are medulloblastomas categorized?

A

either histologically (classic, desmoplastic/nodular, medulloblastoma with extensive nodularity, large cell/anaplastic medulloblastoma)

OR

genetically (WNT activated, SHH activated, non WNT or SHH group 3 and 4)

174
Q

What is the treatment for medulloblastoma?

A

surgical resection of as much as possible, followed by whole-neuraxial radiation and sometimes chemotherapy

175
Q

What are pilocytic astrocytomas?

A

low-grade astrocytic tumors in children and young adults that are found in the cerebellum, optic nerve/chiasm, hypothalamus (in kids) or the cerebral hemispheres or cerebellum (in adults)

176
Q

What are the gross and histological features of pilocytic astrocytoma? Imaging?

A

Gross: well-demarcated and cystic

histology: has long rosenthal fibers (brightly eosinophilic) and microcysts
imaging: solid and cystic mass, usually contrast enhancing

177
Q

What are the typical symptoms of pilocytic astrocytomas?

A

gait and ipsilateral limb ataxia (if in cerebellum)

cognitive and behavioral abnormalities with endocrine dysfunction (if in hypothalamus)

visual field defects and blindness (if in optic nerve)

178
Q

What is craniopharyngioma?

A

tumors believed to arise from the remnants of Rathke’s pouch (embryonic precursor of anterior pituitary, oral mucosa, and teeth)

usually in a pseudocapsule above the sella turcica and include compression of third ventricle, increased ICP, and endocrine dysfunction

179
Q

What characteristic visual abnormality accompanies craniopharyngioma?

A

bitemporal hemianopsia

180
Q

What is the pathophysiology of metastatic/secondary CNS tumors?

A

must develop its own blood supply –> invade local tissues –> enter circulation and reach venous circulation –> hits the lung first (usually first spot of metastases) –> must grow in lung and seed the pulmonary venous circulation to be sent to the brain by the heart

181
Q

What two factors promote metastases to the brain?

A
  • brain gets a ton of the body’s overall blood flow
  • brain is a good spot for arrest and growth (protected from immune, good blood supply)
182
Q

What are supportive care tools for metastatic brain cancer?

A

corticosteroids - for symptoms

anticonvulsants - for symptoms

anticoagulants - thromboembolic disease more likely with cancer

183
Q

What are disease modifying treatments for brain metastases?

A
  • surgery
  • radiation therapy
  • radiosurgery
  • chemotherapy
  • prognosis is usually very poor*
184
Q

Which of the following frequently present with seizures:

high grade glioma, low grade glioma, PCNSL, meningioma

A

low grade glioma = meningioma > high grade glioma

PCNSL can also cause seizures

185
Q

Which of the following frequently present with focal neurologic deficits:

high grade glioma, low grade glioma, PCNSL, meningioma

A

high grade glioma > PCNSL

low grade glioma and meningioma can also cause this but less likely

186
Q

Which of the following frequently present with cognitive/behavioral changes:

high grade glioma, low grade glioma, PCNSL, meningioma

A

PCNSL > high grade glioma > meningioma (least likely)

187
Q

How do brain tumors present clincally?

A

both focal neurologic symptoms as well as generalized neuro symptoms from high ICP

188
Q

What does contrast enhancement on neuro-imaging indicate?

A

blood brain barrier breakdown

189
Q

Why should brain tumor patients with seizures not receive enzyme inducing anticonvulsants?

A

these may interfere with chemotherapy

190
Q

What genetic abnormality/tumor marker is seen in oligodendroglioma?

A

1p19q codeletion

191
Q

Why does glioblastoma often have a classic “butterfly” appearance on MRI?

A

it grows and spreads via white matter tracks, including the corpus callosum that gives the “butterfly” appearance

192
Q

Why do meningiomas enhance homogenously after the administration of IV contrast?

A

because they lie outside the BBB

193
Q

Why can’t many gliomas be surgically resected completely?

A

because they may be growing in “eloquent” cortex that can’t be cut without damaging the patient’s neurologic state

194
Q

Why aren’t gliomas treated with focal radiotherapy instead of whole brain radiotherapy?

A

because wbrt would cause more risks without benefit

195
Q

What is the standard surgical approach for a patient suspected of having a primary CNS lymphoma?

A

biopsy only

196
Q

Where do medulloblastomas originate from?

A

vermis of the cerebellum usually

197
Q

How can you differentiate craniopharyngioma from pituitary adenoma on imaging?

A

calcification with craniopharyngioma (best seen on CT head)

198
Q

What visual field defects do patients with pituitary adenoma present with?

A

bitemporal hemianopsia

199
Q

What syndrome is bilateral CN VIII schwannomas pathognomonic for?

A

neurofibramatosis type 2

200
Q

In what tumor are Rosenthal fibers found?

A

pilocytic astrocytoma

201
Q

Why do patients with medulloblastoma often present with signs of increased intracranial pressure?

A

from obstruction of the 4th ventricle due to tumor growth

202
Q

Which tumor type has “pseudopallisading necrosis” microscopically?

A

glioblastoma

203
Q

What is the mechanism whereby corticosteroids reduce symptoms in primary or secondary brain tumors?

A

by reducing vasogenic edema

204
Q

How do leptomeningeal metastases present?

A

with both focal and generalized symptoms, also classically cranial nerve and spinal nerve findings/symptoms

205
Q

hy do patients with leptomeningeal metastases develop headache and signs of increased intracranial pressure?

A

because of abnormal CSF absorption from tumors interfering with arachnoid granulations and normal CSF reabsorption

206
Q

Which tumor type has psammomabodies on histology?

A

meningioma

207
Q

What are signs of increased intracranial pressure?

A

headache, nausea, vomiting

208
Q

What is the appearance of a meningioma on MRI?

A

homogenously enhancing dural based tumor with enhancing dural tails

209
Q

What is the role of surgery in gliomas?

A

for diagnosis and treatment

greater extent of resection leads to better prognosis

210
Q

What are the most common pediatric tumors?

A

medulloblastoma, ependymoma

211
Q

What is nystagmus?

A

rhythmic pattern of a slow phase of eye movement, followed by a fast phase of eye movement that is oppositely directed

direction of nystagmus designated by the direction of the fast phase movement

212
Q

What is vestibular neuritis?

A

inflammation of the vestibular nerve

213
Q

What is the physiology of the vestibular sensory cells?

A

“hair cells” function as motor sensors by converting movement into an electrical signal

each hair cell has a specific orientation (meaning movement one way may lead to increased firing while movement another way may lead to decreased firing) and is paired with a cell with the opposite polarity

the difference in firing rates between each hair cell is processed by the vestibular nuclei and sends signals to oculomotor nuclei to drive eye movements

214
Q

What is the effect of rotation of the head around the vertical axis on hair cells in the horizontal semicircular canals?

A

turning head causes increased firing ipsilaterally and decreased firing on the contralateral side (push-pull relationship)

215
Q

What is the pathophysiology of eye movement in vestibular neuritis?

A

damage to vestibular nerve reduces rate of electrical signaling coming from the inner ear on that side

this causes eyes to drift towards the side affected by vestibular neuritis at first, and then snapping back to the target (the snap back direction = direction of the nystagmus)

216
Q

What is the treatment for vestibular neuritis?

A

acute phase: manage symptoms (dizziness, anti-emetics)

later: vestibular rehabilitation therapy

217
Q

What is the dix-hallpike maneuver?

A

A maneuver to test for vestibular function where a patient’s head is tilted and then the patient’s upper body is lowered flat quickly

tests for benign paroxysmal positional vertigo

218
Q

What is the pathophysiology of benign paroxysmal positional vertigo?

A

otoconia (crystals) reside in the parts of the inner ear labrynth (utricle and saccule) under normal conditions

sometimes the crystals can break off and enter the semicircular canals and stimulate the cristae ampullaris of the semicircular canals, leading to the sensationof dizziness and nystagmus

219
Q

What is the treatment for benign paroxysmal positional vertigo?

A

vestibular maneuvers that guidethe patient’s head through a series of positions to use gravity to coax loose otoliths out of the semicircular canal and back to the saccule/utricle

most common maneuver called the Epley maneuver (for the posterior canal)

220
Q

What is gentamicin ototoxicity?

A

gentamicin (and some other aminoglycoside antibiotics) are preferentially vestibulotoxic

they accumulate slowly and can have toxic effects that persist to weakness or complete loss of the vestibular hair cells

symptoms can improve despite permanent loss of cells due to multisensory integration

221
Q

What is the physiology of multisensory integration?

A

incorporation of multiple sensory modalities (vestibular function, vision, somatic sensation, proprioception) to understand the body’s orientation and movement through space

normally these inputs are prioritized and weighted based on what position is most likely, but if one of them is lost the others can help compensate

222
Q

What is the pathophysiology of motion sickness?

A

a nauseous feeling that can arise when multisensory integration fails to reconcile inter-sensory discrepancies

223
Q

What is the treatment for motion sickness?

A

vestibular suppressants (dimenhydrinate, meclizine)

224
Q

What is the histologic criteria for grading glial tumors?

A

AMEN

Atypia

Mitoses

Endothelial/vascular proliferation

Necrosis

225
Q

What are the histologic findings of infiltrating astrocytomas?

A

increased cellularity, infiltration of cortex by atypical astrocytes

mitoses, vascular proliferation and necrosis (higher grade tumors)

226
Q

What genes are associated with astrocytomas?

A

isocitrate dehydrogenase genes

227
Q

What is the most common location of pilocytic astrocytomas?

A

cerebellum (most common)

can also be in thalamus/hypothalamus/third ventricle, optic nerves, cerebral hemisphere, and spinal cord

228
Q

What are the imaging, gross, and histologic findings of pilocytic astrocytoma?

A

imaging: cyst with enhancing mural nodule
gross: well-circumscribed, well-demarcated from adjacent brain parenchyma
histologic: well-circumscribed, minimal infiltration at edges of tumors, biphasic (compact areas of rosenthal fibers, loose/microcystic areas)

229
Q

What are the histologic findings of grade 2 and grade 3 oligodendrogliomas?

A

Grade 2: sheets of cells with round, uniform nuclei with a moderate amount of clear cytoplasm with a background of “chicken wire” capillaries with microcalcifications

Grade 3: same as 2 but with increased nuclear atypia, increased mitoses, epithelial proliferation and/or necrosis

230
Q

What are the histologic findings of ependymomas?

A

round to oval, uniform nuclei and eosinophilic cytoplasm

forms perivascular “pseudorosettes” or true ependymal rosettes

231
Q

What are the histologic features of medulloblastoma?

A

large, hyperchromatic nuclei and scant cytoplasm, nuclear molding

may form Homer-Wright rosettes

232
Q

What genetics are associated with atypical teratoid/rhabdoid tumors?

A

loss/mutation of hSN5/INI1 gene on chromosome 22

233
Q

Which of the following tumors shows increased mitoses, microvascular proliferation, and pseudopalisading necrosis?

a) glioblastoma, WHO grade 4
b) oligodendroglioma, WHO grade 2
c) diffuse astrocytoma, WHO grade 2
d) anaplastic astrocytoma, WHO grade 3
e) ependymoma, WHO grade 2

A

a) glioblastoma, WHO grade 4

234
Q

Which of the following primary neuroepithelial neoplasms represents a non-infiltrating lesion:

a) anaplastic astrocytoma
b) anaplastic oligodendroglioma
c) glioblastoma
d) diffuse astrocytoma
e) pilocytic astrocytoma

A

e) pilocytic astrocytoma

235
Q

Perivascular pseudo-rosettes and true rosettes are most diagnostic of:

a) oligodendroglioma
b) ependymoma
c) pilocytic astrocytoma
d) diffuse astrocytoma
e) glioblastoma

A

b) ependymoma

236
Q

What type of tumor is this?

A

Astrocytoma

top = diffuse GII, bottom = anaplastic GIII

237
Q

What type of tumor is this?

A

oligodendroglioma

238
Q

What type of tumor is associated with ependymal rosettes/pseudorosettes?

A

Ependymoma

239
Q

What type of tumor is this?

A

Ependymoma

240
Q

Which type of tumor is associated with bi- and multinucleate, dysmorphic neurons?

A

Ganglioglioma

241
Q

What type of tumor is associated with Homer-Wright rosettes?

A

Medulloblastoma

242
Q

What type of tumor is this?

A

Medulloblastoma

homer-wright rosettes

243
Q

What type of tumor is this?

A

Meningioma

244
Q
A

a) glioblastoma

pseudo palisading necrosis associated with higher grade tumors

245
Q
A

D) oligodendroglioma

246
Q

Perivascular pseudorosettes and true rosettes are most diagnostic of:

a) oligodendroglioma
b) ependymoma
c) pilocytic astrocytoma
d) medulloblastoma
e) glioblastoma

A

b) ependymoma

247
Q
A

E) meningioma

248
Q

Which of the following primary neuroepithelial neoplasms represents a relatively discrete type of lesion?

a) anaplastic astrocytoma
b) anaplastic oligodendroglioma
c) glioblastoma
d) medulloblastoma
e) pilocytic astrocytoma

A

e) pilocytic astrocytoma

249
Q

What are the two types of territories affected by an arterial occlusion stroke?

A
  • area of brain entirely supplied by the artery (core of the ischemic stroke)
  • area fed jointly by more than one arteries (perfusion lesion)
250
Q

What are the treatments for an acute stroke?

A

reopen the occluded artery: thrombolytic agents by vein (main approach), can also do a more aggressive revascularization therapy (less common, reduced evidence)

251
Q

How are recurrent strokes prevented?

A

Identify the cause of the first stroke and alleviate the cause (ex. reduce clotting if the problem was an emboli)

252
Q

What is the mechanism of a small vessel occlusion stroke?

A

occlusion due to microatheroma or lipohyalinosis of penetrating arteries in the basal ganglia, internal capsule, thalamus, or pons

occurs due to hypertension, diabetes, and smoking

253
Q

What is the treatment for small vessel occlusion strokes?

A

antiplatelet medications (aspirin), statins, and blood pressure control

254
Q

What is the mechanism of large vessel cervical artery disease?

A

Occlusion or stenosis of the cervical carotid or vertebral arteries

255
Q

What is the treatment for large vessel cervical artery disease?

A

risk factor control

if carotid stenosis, endarterectomy or stenting

256
Q

What is the mechanism of intracranial atherosclerosis? Treatment?

A

mechanism: occlusion or stenosis of the intracranial vessels of the circle of Willis
treatment: risk factor control, antiplatelet therapy, and (rarely) angioplasty and stenting

257
Q

What is the mechanism of cardioembolic strokes? Treatment?

A

mechanism: stroke due to embolization of thrombus or other material from the heart, often secondary to afib, low ejection fraction, cardiac thrombus, recent MI, or tumors
treatment: anticoagulation with warfarin (or others)

258
Q

What is the typical presentation of a stroke patient?

A

older man with hypertension and afib, not on blood thinners

suddenly stops speaking, limp on one side, fall out of chair

awake patient, no speech, no comprehension, no blinking on weakened side, hemiplegia

259
Q

What are clinical predictors of stroke risk at 90 days post-transient ischemic attack?

A
  • age > 60
  • BP > 140/90
  • clinical features (hemiparesis, speech)
  • diabetes
  • duration > 10 min
260
Q

What is a lacunar stroke?

A

A stroke from one of the small arteries that provides blood to the brain’s deep structures

261
Q

What are the symptoms of a left anterior cerebral artery stroke?

A

right leg weakness (motor cortex medially)

right leg numbness (sensory cortex)

difficulty initiating verbal responses (prefrontal cortex and supplementary motor area)

262
Q

What are the symptoms of a left middle cerebral artery stroke?

A

right face and arm > leg weakness (motor cortex/CST)

right sided sensory neglect (sensory cortex/parietal dysfunction)

global aphasia (Broca’s and Wernicke’s area)

263
Q

What are the symptoms of a right posterior cerebral artery stroke?

A

left visual field homonymous vision loss (visual cortex)

left sided numbness (thalamus)

264
Q

What are the symptoms of a left retinal artery stroke?

A

left eye painless vision loss (amaurosis fugax)

265
Q

What are the symptoms of a lacunar stroke of the right internal capsule, posterior limb?

A

pure motor hemiparesis

pure sensory loss

ataxic hemiparesis

clumsy-hand dysarthria

266
Q

What are the symptoms of a basal artery penetrator stroke?

A

left hemiparesis (from right corticospinal tract)

right hemiataxia (from right pontine nuclei)

dysarthria (right corticobulbar tract)

267
Q

What are the symptoms of a right posterior inferior cerebral artery stroke?

A

right dysmetria and ataxia (cerebellum)

headache (pressure)

nausea/vomiting (area postrema)

dizziness (vestibular connections)

268
Q

What are the locations of intracranial hemorrhage?

A

subarachnoid, subdural, intraventricular, intraparenchymal

269
Q

What is the most common risk factor for intracranial hemorrhage?

A

hypertension

270
Q

What is a traumatic brain injury?

A

nondegenerative, noncongenital insult to the brainfrom anexternal mechanical force, possibly leadingto permanent or temporary impairment of cognitive, physical, and psychosocial functions, with an associated diminished or altered state of consciousness

271
Q

How are potential traumatic brain injuries evaluated?

A

quick neuro exam, CT scan without contrast, consider intubating if neuro exam shows significant findings

272
Q

What are the components of the Glascow coma score?

A

eye opening (4 - spontaneous, 1 - none)

motor response (6 - follows commands, 1 - none)

verbal function (5 - oriented x3, 1 - no response)

consider intubation if < 8

273
Q

What are intraparenchymal hemorrhages?

A

“bruising” of the brain, often of the bilateral frontal lobe

can “blossom” over time

274
Q

What is the most common etiology of subdural hematoma?

A

bridging veins

275
Q

What is the usual cause of epidural hematoma?

A

injury to middle meningeal artery from temporal bone fracture

276
Q

What are the imaging features of diffuse axonal injury?

A

CT looks pretty normal

need specialized imaging to see

277
Q

What is chronic traumatic encephalopathy?

A

progressive neurodegeneration associated with repetitive head trauma

Neuro (12 decks)

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