9/20/2013 Flashcards

Question

Blood supply of brain

Answer 1

Anterior circulation (forebrain) – Anterior and Middle Cerebral Arteries ## Footnote Posterior circulation (posterior cerebral cortex, thalamus, and the brainstem) – Posterior cerebral, basilar, and vertebral arteries

Answer 2

Lenticulostriate arteries and Anterior Choroidal arteries (branches of middle cerebral)

Answer 3

Septum Pellucidum – separates the anterior horns of the lateral venricles Lateral Surface – Basal Ganglia Thalamus is the wall around 3rd Ventricle

Answer 4

o Immediate flaccidity of muscles on contralateral side (above crossing)  Spinal shock – immediate decrease in spinal circuits because of lack of input from motor cortex and brainstem o Acute manifestations tend to be most significant in arms and legs o Trunk muscles usually preserved (brainstem pathways and bilateral projections of the anterior corticospinal tract that controls the midline) o Several days after, the picture changes  Positive Babinksi (extensor instead of flexor) and Hoffman  Spasticity – increased muscle tone (resting muscle tension) because the efferent fibers are much more sensitive to stretch afferents, hyperactive reflexes (and clonus) due to loss of inhibition from UMNs; tested clinically by increased resistance to passive movement • Much more severe stiffness when it follows damage to cortex/internal capsule than in spinal cord - if brainstem descending control is still intact, it exerts net excitatory effect (lesions above the spinal cord will leave brainstem paths intact)  Decerebrate rigidity (extensor muscles of the leg and flexor muscles of the arm), slowness of movement  Loss of ability for fine movements

Answer 5

o Flaccid paralysis/weakness to muscle depending on extent of injury o Loss of muscle tone because of injury to alpha motor neurons (the reflex circuit is normally responsible for steady level of tension in muscles) and hyporeflexia o Fasciculations (loss of innervation leads to muscles producing more Ach receptors, more spontaneous firing) o Eventually, muscle atrophy (not receiving direct innervation)

Answer 6

o Usually asymmetric o Usually distal o Atrophy, fasciculation, cramps o Neuropathies have a single large action potential when fired (due to regeneration of nerve fibers that are not as diversified) – unlike smooth movement that is produced by many action ptoentials

Answer 7

o Usually fluctuating and fatigable

Answer 8

o Usually proximal o Usually symmetric o Usually painless o Usually non-fluctuating o Myopathies have smaller action potential when fired

Answer 9

Quadriceps

Answer 10

Foot dorsiflexion

Answer 11

Plantar flexion

Answer 12

Sphincter control

Answer 13

Injury to nerve roots - LMN

Answer 14

Injury to spinal cord – UMN

Answer 15

Fib – Individual muscle fiber that spontaneously fires (up--regulation of Ach receptors); not visible ## Footnote Fas – Muscle fiber group that visibly contracts (common in peripheral motor nerve injury) – may be due to re-innervation; may not always indicate a pathology

Answer 16

Akinesia – lack of purposeful movements Bradykinesia – Slow movements

Answer 17

Clasp-knife – sudden loss of rigidity at the end of external flexion Cogweel – catch and release Lead pipe – increased tone throughout passive movement

Answer 18

Injury to STN (infarct, tumor, surgery) – loss of indirect pathway, loss of inhibition Uncontrolled flinging movements Treated with dopamine agonists

Answer 19

Triad – Tremor, Rigidity, Bradkykinesia Braak’s Hypothesis: Pre-motor (loss of smell, sleep issues, constipation)  Motor  Dementia, Neuropsychiatric issues Neurodegenerative disease of substantia nigra pars compacta 10% Genetic

Answer 20

100% Genetic – Triplet (CAG) repeat for glutamine, longer the repeat, the earlier the onset, autosomal dominant (toxic gain of function) Degeneration of caudate and putamen, selectively for indirect pathway (loss of inhibition) Many neuropsychiatric issues, late stage akinesia (ablation of cortex, brain as a whole)

Answer 21

Presentation – Sudden headache “worst I’ve had in my life” – possibly due to irritating the Circle of Willis with nuchal rigidity Lumbar puncture shows xanthochromia (yellow due to RBCs entering the CSF; when RBCs die, they release heme, which is degraded by enzymes into the yellow bilirubin) Causes: Rupture of Berry aneurysm, AVM, and an anti-coagulated state

Answer 22

Most frequent cause of subarachnoid hemorrhage (85%) Thin-walled out-pouching that lack a media (note intracranial arteries, in contracts to extra-cranial counterparts, have a smaller tunica media and lack external elastic lamina; this is particularly true at branch points where there is not a well-developed media layer), increasing its rupture risk Most frequently located in the anterior circle of Willis at branch points of the communicating artery; posterior communicating might impinge on VIII Associated with Marfan syndrome and autosomal dominant polycycstic kidney disease

Answer 23

Acute, bilateral paralysis: A patient is aware and awake but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for the eyes. ## Footnote Causes:1) Stroke - Infarction of ventral pons, generally due to basilar artery embolism or thrombosis 2) Central pontine myelinolysis (demyelination disease that affects anterior of pons where the corticospinal tracts are) secondary to rapid IV correction of hyponatremia Risk Factors: Alcoholics, Liver Disease Pathogenesis: Lowered osmolytes in the brain cannot be as quickly replaced as the extracellular osmolarity increases, which leads to shrinkage of brain/loss of fluid from inside cells; the mechanism by which a rapid fall in brain volume results in demyelination is not completely understood. One possible mechanism is that osmotic shrinkage of endothelial cells opens the blood-brain barrier, allowing the entry of complement and other cytotoxic plasma components. Another proposed mechanism is that, during recovery from hyponatremia, the loss of cell water coupled with the movement of potassium and sodium back into the cells leads to an initial increase in cell cation concentration that occurs before the repletion of organic osmolytes. These combined changes may directly injure and induce apoptosis of astrocytes, leading to a disruption in the function of myelin-producing oligodendrocytes, release of inflammatory cytokines, and activation of microglia.

Answer 24

The degree of cerebral edema and therefore the severity of neurologic symptoms are much less with chronic hyponatremia . This protective response, which begins on the first day and is complete within several days, occurs in two major steps. ## Footnote 1) The initial cerebral edema raises the interstitial hydraulic pressure, creating a gradient for extracellular fluid movement out of the brain into the cerebrospinal fluid 2) The brain cells then lose solutes, leading to the osmotic movement of water out of the cells and a decrease in brain swelling. Substantial depletion of brain organic osmolytes occurs within 24 hours, and additional losses occur over two to three days owing to downregulation of the synthesis and uptake of these solutes

Answer 25

Due to rupture of atherosclerotic plaque Usually develops at branch points (e.g. bifurcation of internal carotid and middle cerebral artery) Results in pale infarct at the periphery of the cortex

Answer 26

Due to thromboemboli, most commonly from the left side of the heart (e.g. secondary to atrial fibrillation) Usually involves middle cerebral artery Results in hemorrhagic infarct at the periphery of cortex

Answer 27

Secondary to hyaline arteriolosclerosis (thickening of arteriole, mostly in kidney, with hyaline), which is a complication of hypertension/diabetes Most common in lenticulostriate (caudate, putamen, globus pallidus) vessels, which are a branch of middle cerebral, which results in small “cystic” areas of infarction Thalamic involvement causes sensory stroke Internal capsule involvement causes motor stroke

Answer 28

Accumulation of pus – dead neutrophils – appear as ring-enhancing lesions on CT scan 60% are related to middle-ear infections Cerebellar abscess is specifically associated with otitis media (think about anatomical location) Middle-ear infection and sinusitis can cause frontal and temporal lobe abscesses

Answer 29

Complete failure of higher brain structures to develop; accompanied by grossly deformed head with no cranial vault

Answer 30

Protrusion of brain and meninges through a developmental defect in the skull

Answer 31

Extreme form of porencephaly in which the cerebral hemispheres are destroyed; unlike anencephaly, the external head forms normally

Answer 32

Cyst or cavity in brain that communicates with ventricles – may occur developmentally, or secondary to inflammatory disease or a vascular accident

Answer 33

Atrophy of rostral vermis most commonly caused by alcohol abuse → gait, trunk and leg dystaxia

Answer 34

Usually result of brain tumors in children (most commonly caused by medulloblastomas or ependymomas), involves flocculonodular lobe → truncal dystaxia

Answer 35

Involves one hemisphere, often result of brain tumor (astrocytoma) or abscess (secondary to otitis media or mastoiditis) → arm, leg and gait dystaxia and ipsilateral cerebellar signs

Answer 36

Affected infants usually die before 1 year of age, usually secondary to multiple congenital anomalies, particularly severe congenital heart defects; other features include holoprosencephaly (forebrain fails to develop into two hemispheres, causing defects in face development), micropthalmia (small eye), microcephaly, cleft lip/palate, polydactyly, congenital heart disease, severe mental retardation

Answer 37

Familial, progressive, bilateral, symmetric postural tremor of the upper extremities that is not typically associated with other neurologic symptoms; generally increases with increasing age and is more prevalent in patients with a positive family history; primarily affects the arms in 6-12 Hz frequency; head (titubation) may also be involved

Answer 38

Cystic degeneration of spinal cord due to an occlusion in the central canal right above the anterior commisure. A syrinx results when a watery, protective substance known as cerebrospinal fluid, that normally flows around the spinal cord and brain, transporting nutrients and waste products, collects in a small area of the spinal cord and forms a pseudocyst (e.g. obstruction in CSF flow caused by Chiari can be redirected to cyst?) Arises with trauma or in association with an Arnold-Chiari malformation Usually occurs at C8-T1 (cervical region) Expansion of cyst (“synrix”) over time leads to involvement of other spinal tracts, leading to muscle atrophy and weakness with decreased muscle tone and impaired reflexes – damage to LMNs. It can also lead to Horner syndrome due to disruption of the lateral horn of the hypo-thalamospinal tract (sympathetic input for face; arises from hypothalamus and synapses on the lateral horn at T1  superior cervical ganglion  eyelids, pupil, skin of face)

Answer 39

Droopy eyelid, miosis, and anhidrosis (decreased sweating) – lack of decreased sympathetic innervation of eye

Answer 40

Syphilitic myelopathy – slow degeneration (de-myelination) of nerves in the dorsal columns of the spinal cords (proprioception, sensation, vibration) Tertiary Syphilis (decades later of untreated syphilis) Argyll-Robertson pupils: Accommodates, but doesn’t react (constrict) to light

Answer 41

The stimulation electrode depolarizes all of the axons in the nerve, causing them to simultaneously fire action potentials. The signal obtained at the recording electrode represents a summation of the action potentials of the individual nerve fibers. It is examined for velocity, amplitude and for the shape of the waveform. Used to detect demyelination, which is shown by: 1) decreased conduction velocity (demyelinated nerves will not be able to pass along the action potential effectively because of decreased resistance and increased capacitance forces – back to current model) 2) decreased signal amplitude (determined by the # of axons firing, so decrease indicates axonal loss or complete conduction block for some of the fibers) 3) Abnormal waveform (due to combo of myelinated and demyelinated fibers)

Answer 42

Peptide – synthesized in cell body; larger (3-36 amino acids) Small molecule – synthesized in nerve terminal (enzymes synthesized in cell body); individual amino acids

Answer 43

Inhibit ACheE; initially an over-stimulation, then paralysis (completely depolarized and cannot be responsive to further innervation)

Answer 44

* Ionotropic cation channel * Need to bind two molecules of Ach (thus, high concentrations needed to activate) * Nicotonic receptors activated by “nicotine” and other toxins (e.g. snake toxin); found in the NMJ and pre-ganglionic synapses

Answer 45

* Metabotropic, mediate most things in the brain, all glands and parasympathetic effector organs * Muscarinic receptors are activated by muscarine, a poisonous alkaloid in mushrooms * Remember – atropine is a muscarinic receptor antagonist!

Answer 46

Follows acute brain injury – neurons in ischemic areas exhibit increased glutamate, which contributes to toxic levels for the cell (mechanism unknown – glutamate receptors literally “excite” neurons to death)

Answer 47

* Outnumber neurons * Astrocytes – maintain appropriate environment for neural signaling * Oligodendrocytes – myelin * Microglial – macrophages

Answer 48

AMPA and NMDA are the big ones; non-selective cation influx Note NMDA: • Mg-block relieved by depolarization (e.g. repetitive firing leads to summation and massive depolarization, role in plasticity) • Requires glycine as co-transmitter • Allows calcium inside the cell, which can serve as a second messenger • Slower-acting than AMPA Most cells have NMDA and AMPA receptors

Answer 49

* Second messenger responses can either be excitatory or inhibitory * Varied roles and responses to pharmacological agents

Answer 50

* Inhibitory (except for developing brains when the concentration of chlorine is higher inside) * Most commonly found in local circuits (also as a projection cell in Purkinje cells of cerebellum) * Date Rape drug causes symptoms due to the byproduct of GABA degradation

Answer 51

* Ionotropic * Influx of chlorine

Answer 52

* Metabotropic * Activates K+ channels * Blocking Ca2+ channels

Answer 53

Ethanol potentiates GABA-receptor actions (treat withdrawal with benzodiazepines); Initially alcohol potentiates GABA receptors, but chronic use causes a down-regulation of GABA receptors and reduced neurotransmission - these changes are responsible for alcohol withdrawal symptoms (increased excitability) and increased reduced tolerance to alcohol

Answer 54

* Inhibitory, very similar to GABA-A (influx of chlorine) * Half of inhibitory synapses in spinal cord use glycine

Answer 55

* Dopamine, Norepinephrine, and epinephrine * All derived from tyrosine

Answer 56

* Substantia Nigra & Ventral Tegmental Area * Actions: Motor, Milk, Mind, eMesis Motivation * Cocaine inhibits DAT * Amphetamines are a stimulus-independent release of dopamine by reversing DAT pump

Answer 57

* Locus Ceruleus * Sleep and wakefulness, attention, and feeding behavior * Note that DBH catalyzes the production of NE from dopamine * Mutation in NET causes orthostatic intolerance (less BP) * Epi is found in brain at lower concentrations than NE, function not known (need PNMT enzyme)

Answer 58

* Tuberomammillary nucleus of hypothalamus * Arousal and attention (anti-histamines make you sleepy) and vestibular function (antagonists of H1 receptor are used for motion sickness; note that H2 receptors are involved in secretion of gastric acid)

Answer 59

* Raphe nuclei (pons and upper brainstem) * Regulate sleep and wakefulness, affect, appetite, aggression, thermoregulation

Answer 60

The level of consciousness or arousability is controlled by an ascending system of connections from the brainstem; two main groups: 1) Cholinergic neurons are active during wakefulness and REM sleep. In the pons, the laterodorsal and pedunculopontine tegmental nuclei (LDT/PPT) project to subcortical targets such as the thalamus. These probably play a role in cortical activation and help produce REM sleep. 2) Neurons of the basal forebrain (nucleus basalis of Meynert, diagonal band of Broca, etc.) use Ach, glutamate and GABA to directly activate cortical and subcortical targets, promoting EEG activation and learning. 3) Monoaminergic neurons are active during wakefulness, slow-down in NREM, and are silent in REM sleep. These project directly to cortex and most subcortical regions. 4) Norepinephrine (NE) – mainly from locus coeruleus (LC); helps promote vigilance and attention 2) Serotonin (5HT) – mainly from raphe nuclei; influences mood 3) 3) Histamine (HIST) – only from tuberomammillary nucleus (TMN); promotes arousal 4) Dopamine (DA) – promotes movement and motivation, but source of wake-promoting DA unclear, possibly ventral periaqueductal grey or ventral tegmental area. 5) The reticular system is a heterogeneous population of midline neurons that extend from the caudal medulla to the midbrain. Mainly, it is an older term that encompasses the wake-promoting systems listed above, but there may be other wake-promoting neurons within this system that have not yet been discovered. Stimulation produces awakening, and lesions produce coma or hyper-somnolence. Peptidergic neurons containing orexin (also known as hypocretin) in the lateral hypothalamus send excitatory projections to all these arousal systems. The orexin system probably helps stabilize wakefulness through activation of all the other arousal regions. People lacking orexin have narcolepsy. Orexin antagonists are being developed as a new treatment for insomnia.

Answer 61

Coma - occurs with lesions of this ascending arousal system or with diffuse, bihemispheric dysfunction

Answer 62

* unconscious but cortex active, dreaming, paralysis of all muscles except respiratory and oculomotor, saccadic eye movements (activity of PPRF), penile/clitoral tumescence, possibly memory consolidation function, increased pulse, increased blood pressure, * 25% of sleep cycle; occurs every 90 minutes, duration increases during the night * Same EEG patterns as wakefulness (fast, low amplitude) * Ach is the principal neurotransmitter; NE/Serotonin reduces REM sleep

Answer 63

Note that ACh major neurotransmitter during REM sleep; aminergic input (e.g. NE, serotonin) will decrease REM sleep

Answer 64

* unconscious with little cortical activity * increased parasympathetic activity * sleep-walking, night-terrors, bedwetting most common during REM stage 3

Answer 65

Ventrolateral preoptic area (VLPO) neurons are active during sleep, and VLPO lesions produce fragmented light sleep. VLPO neurons send inhibitory, GABAergic projections to the TMN and other arousal regions such as the LC and DR. These VLPO neurons are especially active during slow wave sleep and some also continue to fire in REM. VLPO neurons may be activated by sleep-producing chemicals (somnogens) such as adenosine (the effects of which are blocked by caffeine), inflammatory molecules (PGE, etc.)

Answer 66

The EEG is a measure of the summed electrical activity between 2 scalp electrodes. This activity results from extracellular current flows generated by synaptic potentials (EPSP's and IPSP's) in cortical pyramidal cells. During wakefulness, the EEG has a low amplitude and consists predominantly of fast waves. This is due to a lack of synchronized activity across the cortex. High amplitude waves characteristic of deep sleep are due to the synchronized activity of millions of cells. This synchronization arises from the interaction of neurons in the reticular nucleus of the thalamus, thalamocortical relay neurons, and cortical neurons. Frequency of EEG waves parallels wake/sleep state and arousability (“BATS”): Awake (eyes open) – Beta (highest frequency) Awake (eyes closed) – Alpha Stage 1 (Light Sleep) – Theta Stage 2 (Deeper Sleep, Grinding of Jaw) – Sleep spindles\* and K complexes\*\* Stag 3 - (Deepest non-REM sleep) – Delta (lowest frequency, highest amplitude) REM - Beta \*During sleep these spindles are seen in the brain as a burst of activity immediately following muscle twitching. Researchers think the brain, particularly in the young, is learning about what nerves control what specific muscles when asleep. Sleep spindle activity has furthermore been found to be associated with the integration of new information into existing knowledge. \*\*K-complexes have two proposed functions: first, suppressing cortical arousal in response to stimuli that the sleeping brain evaluates not to signal danger, and second, aiding sleep-based memory consolidation.

Answer 67

Total sleep time is highest in children and then plateaus during young adulthood. REM sleep is the predominant sleep state during infancy, gradually decreasing during childhood and then essentially stable throughout adulthood. Slow wave sleep declines with age. This decline in deep sleep probably accounts for why many people wake from sleep more frequently as they age, but people still require the same total amount of sleep through adulthood.

Answer 68

1) Homeostatic control: Prolonged wakefulness will produce longer, deeper sleep with more stage 3 NREM sleep. This is often referred to as the homeostatic component of sleep, the presumption being that sleep mechanisms are trying to restore the brain to some equilibrium. 2) Circadian clock: Sleepiness is dependent on the time of day. If you stay up all night, you feel pretty sleepy around 3 am, but by 10 am that sleepiness is not as intense even though you have been awake longer. This is referred to as the circadian component of sleep. Daily 24 hour rhythms known as circadian rhythms have a strong influence on sleep, wakefulness, body temperature, growth hormone, cortisol, and nearly every biologic parameter. These rhythms are mediated by the suprachiasmatic nuclei, small clusters of neurons just above the optic chiasm. SCN neurons act as a pacemaker with a 24 hour cycle of activity. These neurons receive a direct input from retinal ganglion cells containing the novel photopigment melanopsin (even if you lack cones and rods you can still regulate clock). This luminance signal entrains the pacemaker, synchronizing behavior to the external light-dark cycle

Answer 69

1. Ecological – safer to be asleep than out in the environment 2. Energy conservation – sleep burns fewer calories 3. Memory – many memories are consolidated during sleep, improving performance 4. Cellular restoration – Neurons may require periods of reduced activity

Answer 70

ACh is dominant in REM, Aminergic dominant in non-REM

Answer 71

A. About 15% of the population has long-term problems initiating or maintaining sleep. Short term insomnia occurs in ~30% of people. B. Chronic insomnia is often associated with depression or anxiety, maladaptive behavior (psychophysiological), medications, EtOH and other drugs.

Answer 72

A. Circadian phase delay (staying up late and then sleeping late in AM) is very common in teens and young adults. B. Treated with consistent sleep routine, bright light in AM, sometimes melatonin at night.

Answer 73

A. NREM sleep: sleepwalking, confusional arousals, and night terrors B. REM sleep: REM sleep behavioral disorder (failure of paralysis during dreams), strongly associated with Parkinson’s Disease and similar disorders.

Answer 74

Obstructive sleep apnea: upper airway occlusion during sleep due to obesity, small airway, allergies, etc. Treatment: CPAP, surgery, dental device, weight loss. ## Footnote From FirstAid: • Repeated cessation of breathing \> 10 seconds during sleep, which causes disruption and daytime sleepiness • Note that increased hypoxia will leap to more EPO, higher hematocrit • Central – no respiratory effort (medulla isn’t sensing CO2) – headache early morning (would they wake up?) • Obstructive – respiratory effort against airway obstruction, associated with obesity, loud snoring, systemic/pulmonary hypertension, arrhythmias, and possibly sudden death

Answer 75

1) No medial-lateral anatomical organization like somatic motor 2) LMNs are located OUTSIDE of the CNS in paravertebral or prevertebral ganglia 3) Diffuse contacts between the visceral motor neurons and viscera (axons are highly branched and contain varicosities 4) Whereas motor is controlled by the motor cortical areas in the posterior frontal lobe, much more diffuse control “central autonomic network” 5) Diverse NTs

Answer 76

Pre-ganglionic nucleus in midbrain that synapses on the ciliary ganglion via the oculomotor nerve to mediate the parasympathetic constriction in response to light

Answer 77

Pre-ganglionic nuclei in the pons and medulla that mediate the parasympathetic production of tears/salivary glands via VII and IX

Answer 78

Medulla pre-ganglionic nucleus – motor innervation of the pharynx, larynx, and upper esophagus via X and IX

Answer 79

Medulla pre-ganglionic nucleus of X – sends autonomic fibers to the heart, lungs, and upper GI

Answer 80

Sympathetic ganglion have more dendrites and more fibers converge onto it than parasympathetic ganglia

Answer 81

Sweat glands, adrenal medulla, piloerector muscles, most arterial blood vessels

Answer 82

Also known as Aeurbach’s Plexus – intrinsic to gut Between the two muscle layers Regulates the musculature of the gut

Answer 83

Also known as Meissner’s Plexus Located in submucosa, concerned with glandular secretion and chemical monitoring

Answer 84

1) Provides feedback input to local reflexes that modulate moment-to-moment visceral activity within individual organs 2) Informs higher integrative centers of more complex patterns of stimulation that may signal threatening conditions or require coordination of other things

Answer 85

Central structure in the brainstem (medulla) that receives visceral sensory information (includes chemoreceptor and baroreceptor) and distributes it accordingly

Answer 86

1) Far fewer visceral sensory neurons than somatic 2) In the dorsal horn, many of the second-order neurons that receive visceral sensory input (goes through DRG) are part of the anterolateral system, which also receives nociceptive input from more superficial surfaces – pain from viscera can be “referred” to these areas

Answer 87

Outdated term; refers to the heterogeneous collection of distinct neuronal clusters in the brainstem tegmentum that modulate the excitability of neurons in the forebrain and spinal cord or coordinate the firing patterns of more local lower motor neuronal pools engaged in reflexive or stereotypical somatic motor and visceral motor behavior (e.g. PPRF) ## Footnote Broadly speaking, modulatory functions are found in the rostral sector and premotor functions are localized in more caudal regions

Answer 88

Nucleus of solitary tract Visceral motor centers in the medullary reticular formation Sensory fibers related to viscera convey limited amount of information to consciousness (except pain)

Answer 89

Cell bodies in the DRG (spinal visceral sensory neurons) and sensory ganglia associated with IX and X (i.e. general visceral sensory information from organs and viscera in the thorax, upper abdomen, head and neck; in the abdomen, visceral afferents generally follow pathway of sympathetic nerves)

Answer 90

Some afferent fibers via DRG synapse in the lateral horn where the visceral motor neurons are located

Answer 91

Some pain fibers, especially visceral pain fibers, ascend in the dorsal column and terminate in the dorsal column nuclei and eventually are relayed to thalamus

Answer 92

Responsible for planning and selecting movements, esp. movements that are triggered by sensory cues or internal motivations (the primary motor cortex on the other hand is more involved with the direct execution of skilled movements of the limb and facial muscles)

Answer 93

Sensory inputs (visceral and somatic, chemosensory, and humoral) + Contextual information (cerebral cortex, amygdala, hippocampal formation) ## Footnote Compares input to biological set-point; Output to visceral motor (autonomic premotor centers in brainstem and pre-ganglionic neurons in brainstem and spinal cords), somatic motor, neuroendocrine, behavioral responses

Answer 94

Ptosis, Miosis, Sunken Eye, Decreased sweating (if the descending pathway is affected)

Answer 95

Nicotonic/Pre-ganglionic: Fast (ion channel) Muscarinic/Adrenergic/Post-ganglionic: Slower (G-proteins)

Answer 96

Periaqueductal Grey – when socially acceptable, there is increased parasympathetic outflow (S2, S3, S4) and disinhibition of the skeletal muscle of the sphincter (S2, S3, S4)

Answer 97

Incomplete bladder emptying – no dishinibition of the motor neurons and/or not enough increased para-sympathetic activity; this leads to chronic UTIs in paraplegic patients

Answer 98

NO released by parasympathetics causes filling of the cavernous venous sinuses (also glandular secretions); afferent stimulation conveyed centrally through somatic sensory endings, which causes increased parasympathetic response and somatic excitation in certain muscles, which causes orgasm

Answer 99

Hypothalamus Supraoptic Area Synthesizes ADH, oxytocin, CRH (Corticotropin-releasing hormone)

Answer 100

Hypothalamus Supraoptic Area Temperature regulation (heat dissipation); lesion leads to hyperthermia (body produces more heat than it is able to dissipate)

Answer 101

Hypothalamus Releases gonadotropic hormones. Sexual dimorphic nucleus, which has a role in sexual behavior, mating, and partner preference. Lesion leads to arrested sexual development, impotence, amenorrhea.

Answer 102

Pre-Optic ## Footnote Regulates circadian rhythms (e.g. cyclic release of CRH, melatonin from pineal gland). Input from retina (melanopsin), output to pineal gland.

Answer 103

Hypothalamus, Tuberal Region. ## Footnote Almost all major pathways feed into this nucleus; also regulates autonomic function(s); stimulation can lead to obesity

Answer 104

Hypothalamus Posterior Temperature regulation (heat conservation). Lesion leads to poikilothermia (poor thermoregulation). Stimulates the sympathetic nervous system.

Answer 105

Hypothalamus Posterior Feeding center. Stimulation leads to increased eating (lateral nucleus causes you to grow laterally). Lesion leads to starvation.

Answer 106

Hypothalamus Posterior Damaged in Wernicke Encephalopathy/Korsakoff psychosis (confabulation, amnesia, ataxia). The circuit is from hypothalamus to fornix to mammillary body.

Answer 107

Hypothalamus Tuberal Region Satiety Center. Stimulation leads to decreased eating (ventromedial nucleus causes you to shrink medially). Lesion leads to obesity, hyperphagia, “savage” behavior

Answer 108

Hypothalamus Tuberal Region Produces hypothalamic releasing and inhibiting factors that act on the anterior pituitary. Inhibits prolactin release via dopamine (aka prolactin-inhibiting factor).

Answer 109

Visuospatial Deficit – medial/lateral parietal lobe lesion (“what” and global impressions) • Simultanagnosia (inability to perceive parts of a complex visual scene as a whole) • Deficits in visually guided reaching (optic ataxia) • Difficulty in voluntary scanning of visual scenes (ocular apraxia) ## Footnote Notably, the ataxia and apraxia disappear when guided by non-visual cues, which suggests that the parietal cortex is involved in spatial construction of images that guide both attention and movement.

Answer 110

* Prosopagnosia (difficulty recognizing faces); can be for all familiar objects, too – depends on location of lesion * Fusiform gyrus * Can recognize using other cues (gait, voices, body shape, etc.) * It is likely that there is no single “grandmother” cell, but rather, that there are populations of cells that code for a specific face depending on orientation, etc. “recognition neurons”

Answer 111

* Difficulties with language-related material (Wernicke’s area) * Lateral surface of the cortex

Answer 112

• Usually symptomatic bilaterally • Impaired restraint • Disordered thought • Perseveration • Inability to plan appropriate action • Working memory impaired (pre-frontal cortex); delay-associated neurons Frontal lobe is involved in the selection, planning, and execution of socially acceptable behavior

Answer 113

• Ability to attend to, identify, and act meaningfully in response to stimuli

Answer 114

* Ability to produce language with appropriate grammar efficiently is disrupted, even though individual knows what they want to say * Motor or Expressive Aphasia * Halting Speech * Tendency to repeat phrases or words * Disordered syntax * Disordered grammar * Disordered structure of individual words, substitution * COMPREHENSION INTACT * REPETITION (is possible of single words perhaps), but difficult

Answer 115

* Difficulty understanding spoken language and producing meaningful content * Sensory or Receptive Aphasia * Most also have difficulty reading and writing, though nearby areas are responsible for this * Receptive aphasia usually have great difficulty understanding the speech of both themselves and others and are therefore often unaware of their mistakes * Fluent, incomprehensible speech * Good grammar * Made-up words * COMPREHENSION not intact * REPETITION is poor

Answer 116

• Posterior part of superior temporal gyrus; that is why Wernick’es aphasia may also be associated with a contralateral upper quadrant field cut (temporal lobes)

Answer 117

• Inferior frontal gyrus; part of pre-motor cortex

Answer 118

* Lesion to pathway connecting B&W * Arcuate Fasciculus * Inability to repeat spoken command (Auditory to W to B to Motor) * COMPREHENSION INTACT * Spontaneous speech is also intact – with some syllabic insertions here and there * REPETITION is impossible

Answer 119

* Broca’s and Wernicke’s is affected * No motor, no repetition, no comprehension

Answer 120

* Deficiency in ability to produce tone * Right side in regions that correspond to Broca’s and Wernicke’s areas

Answer 121

• Inability to move muscles of the face

Answer 122

* Can be visual, auditory, or tactile * Lesion in unimodal association area * Associated with inability to process what (e.g. right temporal lesion causes prosopagnosia)

Answer 123

* Can produce language, but don’t know what they just said (like conduction agnosia?) * Auditory separated from language center (unimodal auditory association lesion)

Answer 124

Arises from lesions in the left angular gyrus (junction of parietal and temporal lobes) – Agraphia – Acalculia – Finger agnosia – Right-left disorientation

Answer 125

AVM malformation

Answer 126

* Intraparaenchymal hemorrhage * Smaller vessels than Berry Aneurysm; affected that run into the deep tissues of the brain (basal ganglia is the most common site) * Often due to hypertension (secondary to hyaline ateriosclerosis - recall it can also cause ischemic cystic infarcts)

Answer 127

* Thrombus * Embolism * Hypo-perfusion

Answer 128

• Mechanical damage to the neurons

Answer 129

• Chronic presentation

Answer 130

* Core zone – immediately deprived of oxygen * Peripheral zone – Ischemic penumbra (reversible – residual perfusion from collateral blood vessels)

Answer 131

* Oxidative Stress: ROS (breakdown of mitochondria); ischemic reperfusion * Apoptotic Pathways: Release of cytochrome C and then release of mitochondria; want to give BCL2 or caspases inhibitors * Glutamate Toxicity (all NT released causes influx of calcium, which will trigger enzymatic activity and degrade cells even more); invest in NMDA antagonist

Answer 132

* Down (IV) and Out (VI) * Droopy (Levator Palpebrae) * Pupil Involvement suggests tumor (impinging on PS fibers) * Diabetic neuropathy can implicate vessels in nerve and not affect pupil

Answer 133

* Hypertropic (elevated slightly) * Head tilt away from the lesion (normally intorts, so extorting) * Fourth nerve has a very long path, tumor can be involved * Loops up when medial * Double vision when reading a book

Answer 134

* Diabetes, Hypertension * Intercranial pressure (90 degree exit off pons into the brain) * Can’t look laterally in the eye that is affected, but medial horizontal movement in other eye is not impaired * Bilateral: Can’t look lateral in either direction

Answer 135

* Unilateral: can’t look medially in the contralateral side of the lesion (e.g. right MLF that connected right VI to left III; left side won’t move medial, but right eye will still look lateral * Bilateral: Can’t look medial in either direction

Answer 136

* Slow, broad tremor of the extremities that occurs at the end of a purposeful movement (no constant frequency) * “Intention Tremor”

Answer 137

• Rhythmic muscle contractions in lower limbs when standing, no known pathology

Answer 138

• Cerebellar tremor may be accompanied by other manifestations of ataxia, including dysarthria (speech problems), nystagmus (rapid, involuntary rolling of the eyes), gait problems and postural tremor of the trunk and neck. Titubation is tremor of the head and is of cerebellar origin

Answer 139

• Motor restlessness (inability to sit still)

Answer 140

• Slow, writing movements which may resemble dystonia

Answer 141

• Proximal, large amplitude chorea (“hemiballism” is usually unilateral)

Answer 142

* Non-rhythmic, unpredictable movements * Involuntary, randomly flowing jerks that are often incorporated into voluntary movement

Answer 143

• Abnormal posture, the result of co-contraction of agonist and antagonist muscles; contractions may also result in twisting or repetitive movements

Answer 144

* Shock-like movements due either to muscle contraction (positive myoclonus) or abrupt loss of muscle tone (negative myoclonus) * Not the same as clonus, which is induced by a reflex

Answer 145

• Purposeless repetition of motor set

Answer 146

• Patterned simple or complex movements, spasm, urge to tic, relief afterward

Answer 147

* Decorticate posturing (flexors in upper extremity, extensors in lower extremity * Dis-inhibition of ruprospinal tract (increased flexion in upper extremities) * Inhibition of lateral corticospinal tract (increased extension in lower limbs)

Answer 148

* Inflammatory Polyneuropathy * Rapidly evolving limb weakness * Symmetric hyporeflexia * Normal sensation (sensory symptoms like pain, numbness, and parasthesias can occur, but the motor symptoms predominate) * Symptoms typically ascend * Frequently follows viral infection * May evolve into complete paralysis with respiratory failure

Answer 149

* Autoimmune disease (mimicry mechanism) * Chronic inflammatory infiltrate * Demyelination of peripheral nerves

Answer 150

• Decerebrate posturing (rigid extension of body all over)

Answer 151

* Transient – confusion, disorientation, etc. for less than 30 minutes or so * Can’t see on imaging * Leads to chronic traumatic encephalopathy * Severe to Moderate develop Alzheimer’s-like

Answer 152

* Hippocampus * Damage makes it difficult to form new memories (anterograde amnesia)

Answer 153

Gq-receptor (increase in IP3 and intracellular Ca); causes contraction

Answer 154

Gi-receptor (inhibit adenylyl cyclase, decrease in cAMP)

Answer 155

Gs-receptor (activate adenylyl cyclase, increase in cAMP)

Answer 156

Gs-receptor (activate adenylyl cyclase, increase in cAMP); causes relaxation

Answer 157

When it is activated by Ach, the nicotinic receptor “opens” and creates a channel for Na/K to flow down respective gradients (K outside, Na inside)  depolarization

Answer 158

Gq-receptor (increase in IP3 and intracellular Ca); causes contraction OR Direct action of a G protein (i.e. no second messenger is involved; in SA node, activation of a Gi protein  binds directly to K+ channels  depolarization  slows the rate of depolarization by making the cell hyperpolarized

Answer 159

* Hemiparalysis of the tongue * Upon protrusion of the tongue (accomplished by genioglossus muscle that attaches to the inferior of the tongue and mandible), the tongue goes to the side of the lesion (stronger muscle is unopposed)

Answer 160

* IX for sensory limb (unilateral) – the side that has a lesion will not respond at all * X for motor limb (bilateral) – side that has a lesion (levator palatini) will not raise the soft palate and the uvula will go to the side that does rise up (opposite side) * Think about it as a consensual response – if IX is lesion, but X is fine, there will be a NORMAL gag reflex on the side of pharynx that does not have the lesion

Answer 161

• III, IV, VI, V-1, V-2

Answer 162

* Note that UMN innervation of VII in the upper half of the face is bilateral so that if you destroy cortical input from one side, the upper facial movement is conserved, but the lower face movement on the contralateral side of the lesion is not * To summarize: You would see deficits in the lower half of the face on the contralateral side

Answer 163

• Will cause total face paralysis on the same side as the lesion (think LMN lesion is on the same side)

Answer 164

Damage to anterior motor horn neurons (fecaol oral -- GI -- Blood to CNS) Presents with LMN signs

Answer 165

Inherited degeneration of anterior motor horn (autosomal recessive in gene that supports growth of MNs) Presents as 'floppy baby" Death within few years after birth

Answer 166

Degenerative disorder of upper (lateral spinal tract) and lower motor neurons (anterior motor horn) of corticospinal tract NO SENSORY INVOLVEMENT Most cases are sporadic in middle-aged adults SOD1 (Zinc-copper superoxide dismutase) mutation is present in some familiarl forms (ROS-mediated damage etiology?)

Answer 167

Degenerative disorder of the cerebellum (ataxia) and spinal cord (loss of vibration, proprioception, and LMN injury) Autosomal recessive; due to expansion of unstable trinucleotide repeat (GAA) in frataxin gene, which is responsible for the synthesis of Fe-S clusters (perhaps impaired ETC, which leads to ROS-mediated damage?) Presents in early childhood; patients are wheelchair bound within a few years Associated with hypertrophic cardiomyopathy

Answer 168

* Slow onset memory loss (begins with short-term and then progresses to long-term memory loss) and then progressive disorientation * Loss of learned motor skills and language * Changes in behavior and personality * Patients are mute and bedridden; infection is a common cause of death * Focal neurologic deficits (e.g. weakness in one arm, etc.) are NOT seen in early disease

Answer 169

1st - Alzheimer’s disease 2nd – Vascular Dementia

Answer 170

APP is a receptor with an unknown function; normally undergoes cleavage (alpha) by a presenilin-coded secretase and is properly turned over; when it undergoes beta cleavage, it results in the formation of ABeta amyloid, which can: • Interfere with synaptic efficiency • Form diffuse plaques and initiate immune response • Cause neurofibrillary tangles to form within neurons • Causes selective neuronal loss (not clear why some neurons are not affected while others are) and several NT defects are found

Answer 171

Memory loss, cognitive dysfunction, with no loss of consciousness; degeneration of the cortex leads to dementia

Answer 172

* Most cases are sporadic and seen in elderly * Risk increases with age (doubles every 5 years after the age of 60) * APOE4 has high risk (less clearance of AB amyloid) * APOE2 has reduced risk (more clearance) * Early onset AD is seen in familial cases (mutation in presenilin 1 or 2 that produces excess AB amyloid) * Down syndrome – APP is on chromosome 21 – commonly occurs by age 40

Answer 173

* Cerebral atrophy with narrowing gyri * Loss of brain mass * Dilation of ventricles secondary to loss of brain volume * NF Tangles * Loss of cholinergic neurons in the nucleus basalis of Meynart (part of arousal symptom – leads to fatigue?)

Answer 174

R/O and at autopsy

Answer 175

Intracellular hyper-phosphorylated Tau proteins; seemed to be caused by the “toxic” AB amyloid neuritic plaques that are formed

Answer 176

Neuritic plaques – extracellular; comprised of hydrophobic, beta-sheet stacked AB amyloid with entangled neuritic processes and can be associated with microglia ## Footnote May deposit around vessels, increasing the risk for hemorrhage

Answer 177

Multifocal infarction and injury secondary to hypertension, atherosclerosis, vasculitis

Answer 178

Cognitive impairment, acutely or sub-acutely, after an acute neurologic event with a stepwise progression is a typical history suggestive of vascular dementia. More associated with depression than AZ

Answer 179

When you have global cerebral ischemia… • Moderate – Layers 3, 5, 6, which could result in dementia • Hippocampus – Loss of memory

Answer 180

Parkinson’s MPTP is a metabolite found in a drug that was metabolized into MPP+, which then blocked the ETC in the mitochondria and generated ROS species; found to cause PK

Answer 181

Tremor Rigidity (Cogwheel) Akinesia/Bradykinesia Postural instability and shuffling gait

Answer 182

Alpha-synuclein (Lewy Body) Can spread to cortical areas in late-disease Parkinson’s and cause dementia

Answer 183

DLB is distinguished from the dementia that sometimes occurs in Parkinson's disease by the time frame in which dementia symptoms appear relative to Parkinson symptoms. Parkinson’s disease with dementia (PDD) would be the diagnosis when dementia onset is more than a year after the onset of Parkinson’s. DLB is diagnosed when cognitive symptoms begin at the same time or within a year of Parkinson symptoms.

Answer 184

Chorea Depression High rate of suicide as a common cause of death

Answer 185

Basically the underlying pathophysiology is not entirely known. It is thought that CSF absorption through the arachnoid granulations may be impaired somehow, but perhaps in a very gradual way, so that even though the ventricles enlarge due to impaired CSF absorption, there is not the observable marked increase in intracranial pressure that you would expect. It may be that ICP increases slightly compared to what would be the patient's baseline, but is still within the normal range.

Answer 186

Dementia in Adults, usually idiopathic Wet, Wobbly, and Wacky ## Footnote The symptoms are explained by compression of white matter fibers that run near the lateral ventricles, when the ventricles enlarge. This explains the gait problem that mostly involves the lower extremities (because descending corticospinal tract fibers carrying information for the lower extremities are the ones that travel farthest along the lateral ventricles on their way to the internal capsule, based on the motor homunculus), the urinary incontinence (because the cortical inhibition of bladder function is located in the medial frontal lobes superiorly, and these fibers also run along the lateral ventricles), and the dementia (because the frontal lobes overall are most affected when the lateral ventricles are enlarged). The possibility that ICP may be slightly increased but still within the normal range is supported by the fact that draining large amounts of CSF (Lumbar Puncture) can help the symptoms in NPH, sometimes immediately and markedly, and this is used as a diagnostic test.

Answer 187

Normal prion protein (PRP-C) in alpha-helix formation in neurons is converted to Beta-pleated conformation (PRP-SC) ## Footnote Conversion can be sporadic, inherited, or transmitted

Answer 188

Pathologic prion protein is not degradable and converts normal protein into pathologic form, causing a vicious cycle

Answer 189

Spongy degeneration (damage to neurons and glial cells is characterized by intracellular vacuoles)

Answer 190

CJD Usually sporadic Can be transmitted through human-infected tissue (e.g. corneal transplant, GH) Presents as RAPID dementia associated with ataxia (cerebellum involved) and startle myoclonus Spike-wave complexes on EEG Results in death in usually \<1 year Varient CJD = bovine – mad cow

Answer 191

Prion disease

Answer 192

The role of the hippocampus and parahippocampal areas are crucial for establishing long-term memories. When sensory input is received it is encoded into short term memory (hippocampus-independent). This information is held in working memory (tested in tasks such as counting backward from 100) and if consolidated (hippocampus-dependent) is stored as long term memory which can later be retrieved. ## Footnote Note that: Implicit (or non-declarative) memory such as learning motor skills is not dependent on the hippocampus. H.M., a man who had his hippocampi (and large amounts of the parahippocampal areas) removed bilaterally for epilepsy could no longer encode new explicit memories. He could learn to ride a bike—he would do better each day but have no memory of riding a bike before. In 1997, an MRI study was done to see the extent of the surgical resection.

Answer 193

DECLARATIVE memory (episodic and semantic; not working) is stored in diffuse cortical sites (think Wernicke’s and fusiform gyrus); notably, it depends on the integrity of medial temporal areas (e.g. hippocampus and parahippocampul gyrus) to encode/consolidate memories Injury to medial temporal areas) will lead to anterograde amnesia - can’t form new memories; accessing old memories may still be intact Damage to specific/widespread cortical areas (e.g. Alzheimer’s) will lead to retrograde amnesia (e.g. Fusiform gyrius and face recognition)

Answer 194

DECLARATIVE memory is stored in diffuse cortical sites (think Wernicke’s and fusiform gyrus); notably, it depends on the integrity of medial temporal areas (e.g. hippocampus and parahippocampul gyrus) to encode/consolidate memories Injury to medial temporal areas) will lead to anterograde amnesia - can’t form new memories; accessing old memories may still be intact Damage to specific/widespread cortical areas (e.g. Alzheimer’s) will lead to retrograde amnesia (e.g. Fusiform gyrius and face recognition)

Answer 195

Memory recall three words Counting backward from 100

Answer 196

Frontal and Temporal Lobes Frontal lobes and BG circuits – manipulation of working memory stored information to perform a task Temporal Lobe circuits – storing information

Answer 197

Medial temporal pole Affected first in Alzheimer’s, then it gets more diffuse (affects short-term memory, then long-term memory); note that basic attention and working memory are required to learn new information

Answer 198

Anterior temporal pole Caused by Herpes Enchephalitis, generally rare Intact recall (medial temporal lobe intact) Difficult learning, however, because there is affected temporal lobe function

Answer 199

PPRF located near the midline in the Pons; connects VI and III via the MLF

Answer 200

The rostral interstitial nucleus is located in the rostral part of the midbrain reticular formation

Answer 201

Two regions of the brain project to gaze centers and are responsible for initiating and accurate targeting of saccades • Superior colliculus of the midbrain (also receive input from dorsal spatial vision pathway to align fovea to correct region of space) • Frontal eye field in pre-frontal cortex UMN in both of these regions discharge prior to saccadic movements

Answer 202

Eyes drift toward the side that is injured (“Look toward a stroke, Look away from a Seizure”)

Answer 203

Concentration, orientation, abstraction, judgment, mood, and inhibition of primitive reflexes ## Footnote Lesion could cause unmasked primitive reflexes such as sucking, grasp, and rooting reflexes

Answer 204

Eyes drift away from the side of hyperactivity (“Look toward a stroke, Look away from a Seizure”)

Answer 205

Working memory and executive function (planning tasks, switching tasks, goal-directed behavior) Circuit with BG (e.g. input is where and what visual information, output through thalamus back to LPFC) Implicated in SZ, PK

Answer 206

Verbal Fluency – working memory, self-monitoring, and cognitive flexibility

Answer 207

Emotional control and regulation and social judgment Sensory input through OFC through BG (with Amygdala input) and Visceromotor output (expression of emotion). Responsible for “gut response”. If this circuit is screwed up, then emotional regulation will change. Lesions leave cognition in absence of feeling.

Answer 208

Initiation and monitoring (e.g. supplementary motor area) ## Footnote Bilateral destruction can cause “abulia” – severed initiative – also called akinetic mutism – subjects are awake and alert, but have no movement and no verbal output

Answer 209

Lesion to the dominant - often left parietal lobe – (usually left is dominant for most people and so a lesion on the right side may not result in neglect)

Answer 210

Alexia – Can’t read Agraphia – Can’t write Reading pathway involves visual input through B/W pathway Writing to dictation pathway involves auditory input through B/W pathway Therefore, if you can’t get to B/W pathway from visual cortex, you will get this lesion; could be caused by PCA lesion

Answer 211

Cohclea to CN VIII to meduallary cochlear nucleus, crosses just prior to the superior olivary nucleus, then travels along the lateral leminscus tract then synapses in the medial geniculate nucleus (MGN) and goes to primary auditory cortex

Answer 212

Unilateral hearing loss with potential deafness

Answer 213

Bilateral hearing loss without deafness (bilateral spread of fibers)

Answer 214

Limbic system circuit that plays a role in memory and emotion; although it is not a true circuit, structures of the circuit contribute to memory and emotional processing that is part of the limbic system The Papez circuit begins with fibers arising from the subiculum of the hippocampal formation, which enter the fornix and travel forward to both the medial and the lateral mammillary nuclei. The medial mammillary nucleus then projects through the mammillothalamic tract to the anterior thalamic nucleus. Recall that the anterior thalamic nucleus also receives a direct projection from the fornix. The anterior thalamic nucleus next projects through the internal capsule to the cingulate gyrus. Finally, a prominent white matter pathway underlying the cingulate gyrus called the cingulate bundle, or cingulum, passes from the cingulate cortex to the parahippocampal gyrus. From the parahippocampal gyrus, projections continue to the entorhinal cortex and hippocampal formation, completing the loop.

Answer 215

Responsible for emotional responses, such as fear response

Answer 216

Ablation of the fear response Kluvey-Bucy Syndrome – Psychic blindness (visual agnosia), personality changes (abnormal docility), hyperorality, hypersexuality

Answer 217

Temporal lobe; often presents with visual hallucinations

Answer 218

Word-finding

Answer 219

PCA branch

Answer 220

Kidney, Breast, and Lung

Answer 221

Above; Child are usually below

Answer 222

Pilocytic astrocytoma, ependymoma, and medulloblastoma

Answer 223

No – they are locally destructive, though

Answer 224

Meningioma

Answer 225

Glial fibrillary acidic protein is an intermediate filament (IF) protein that is expressed by numerous cell types of the central nervous system (CNS) including astrocytes and ependymal cells

Answer 226

Astrocytes

Answer 227

Posterior fossa of cerebellum

Answer 228

1. GFAP 2. Rosenthal fibers

Answer 229

Cyst + mural nodule

Answer 230

Cerebellar granular cells (neuroectoderm)

Answer 231

Cerebellum or posterior fossa

Answer 232

Homer-Wright rosettes

Answer 233

Hydrocephalus

Answer 234

Ependymal cells

Answer 235

4th ventricle

Answer 236

1. Perivascular pseudorosettes 2. Blephoroplasts

Answer 237

Hydrocephalus

Answer 238

Vascular cells

Answer 239

Cerebellum

Answer 240

1. Foamy cells 2. High vascularity

Answer 241

Polycythemia Von Hippel Lindau

Answer 242

Epithelial cells

Answer 243

Rathke’s pouch

Answer 244

Calcifications

Answer 245

Bitempeoral hemianopsia

Answer 246

Astrocytes

Answer 247

Cerebral hemisphere

Answer 248

1. GFAP 2. Pseudopalisading necrosis

Answer 249

“Butterfly”

Answer 250

Arachnoid cells

Answer 251

Convexities of hemispheres

Answer 252

1. Whorled 2. Psommoma bodies (calcifications in whirled pattern)

Answer 253

Dural tail

Answer 254

Seizures or focal signs; express estrogen receptor – more common in adult women

Answer 255

Schwann cells

Answer 256

Cranial or spinal nerves (VIII)

Answer 257

Bilateral acoustic

Answer 258

Hearing loss or tinnitus Associated with NF Type 2

Answer 259

Oligoden- drocytes

Answer 260

Frontal lobe

Answer 261

1. Fried egg cells 2. Chicken-wire capillaries

Answer 262

Often prolactinoma

Answer 263

Leptomeninges (arachnoid and pia)

Answer 264

Group B Strep (Culture mom before birth) E. Coli Listeria monocytogenes

Answer 265

N. Meningitidis (through nasopharynx to blood to CNS)

Answer 266

Headache Nuchal Rigidity Fever Photophobia (most commonly in viral), Vomiting, and altered mental status may also be present ## Footnote Kernig’s, Brudzinksi’s signs (most useful in children): Kernig’s is POSITIVE when the child rolls up in response to stretching the leg upward; Brudzinksi is POSITIVE when legs come up when the head is tilted upward

Answer 267

Low glucose, Neutrophils, Positive Gram Stain Note that CSF glucose is 2/3 of systemic glucose Elevate protein

Answer 268

Lymphocytes with normal CSF glucose

Answer 269

Lymphocytes with decreased CSF glucose

Answer 270

Death – herniation secondary to cerebral edema Hydrocephalus (scarring during healing process), hearing loss, seizures

Answer 271

Compression of brainstem in medullary area that can lead to cardiopulmonary arrest

Answer 272

In this type of hernation, the cingulate gyrus herniates under the falx cerebri, which can compress the anterior cerebral artery

Answer 273

Crushes CN III (down and out with dilated pupil) Compression of PCA can lead to contralateral homonymous hemianopia Rupture of paramedian arteries that perforate from basilar into midbrain and thalamus, causing hemorrhage

Answer 274

Most common leukodystrophy Deficiency of arylsulfatase (autosomal recessive) Inability to degrade myelin, which accumulates in lysosomes of oligodendrocytes

Answer 275

``` Deficiency of galactocerebroside B-galactosidase (autosomal recessive) The Galactocerebroside (a glycosylated phospholipid) accumulates in macrophages ```

Answer 276

Impaired addition of coenzyme A to long chain FAs (X-linked defect) ## Footnote Accumulation of FAs damages adrenal glands and white matter of the brain and Leydig cells of testes

Answer 277

CNS myelin and oligodendrocytes

Answer 278

20-30 years, mostly women, mostly in regions that are far from the equator

Answer 279

Yes, HLA-DR2

Answer 280

Relapsing neurologic deficits with periods of remission Blurred vision in one eye (optic nerve) Vertigo and scanning speech (brainstem) Internuclear opthalmoplegia (MLF) Hemiparesis or unilateral loss of sensation (cerebral white matter, usually periventricular) Lower extremity loss of sensation or weakness (spinal cord) Bowel, bladder, sexual dysfunction (ANS)

Answer 281

Lumbar puncture for increased lymphocytes, increased Ig with oligclonal IgG bands (bands seen when sampling from CSF -- each of the two to five oligoclonal bands seen by protein electrophoresis represent proteins (or protein fragments) secreted by plasma cells, although why exactly these bands are present, and which proteins these bands represent, has not yet been elucidated), and myelin basic protein (destroying the myelin)

Answer 282

A repair process, called remyelination, takes place in early phases of the disease, but the oligodendrocytes are unable to completely rebuild the cell's myelin sheath. Repeated attacks lead to successively less effective remyelinations, until a scar-like plaque is built up around the damaged axons

Answer 283

* Progressive, debilitating encephalitis leads to death * Due to persistant infection of measles virus (infection in infancy, neurological symptoms years later) * Characterized by viral inclusions within neurons and oligodendrocytes

Answer 284

* JC Virus infection of oligodendrocytes (white matter) * Most people are infected – reactivated in AIDS/immunosuppressed patients * Presents with rapidly progressive neurological signs (visual loss, weakness, dementia), leading to death

Answer 285

* Low perfusion (hypotension, athero) * Acute decrease in blood flow (cardiogeneic shock) * Chronic hypoxia (anemia) * Repeated episodes of hypoglycemia (“hypoglycemic stroke”)

Answer 286

• Mild, transient confusion with prompt recovery

Answer 287

• Diffuse necrosis; if survival, then in vegetative state

Answer 288

• Infarcts in watershed areas and damage to highly vulnerable regions (pyramidal neuron in layers 3, 5, and 6, which causes cortical laminar necroses; pyramidal neurons in hippocampus, Purkinje layer of the cerebellum

Answer 289

* Hemorrhagic (easily lyse thrombus, can’t easily lyse thrombus next to plaque) * Thrombus causes pale infarct

Answer 290

* Liquefactive * 12 hours - Eosinephila (degraded proteins, RNA) “Red Neurons” * Infiltration by neutrophils (1 day), Microglia (1 week), Granulation-like tissue (1 month), then results in a cystic space surrounded by gliosis Gliosis is a nonspecific reactive change of glial cells in response to damage to the central nervous system (CNS). In most cases, gliosis involves the proliferation or hypertrophy of several different types of glial cells, including astrocytes, microglia, and oligodendrocytes. In its most extreme form, the proliferation associated with gliosis leads to the formation of a glial scar. The process of gliosis involves a series of cellular and molecular events that occur over several days. Typically, the first response to injury is the migration of macrophages and local microglia to the injury site. This process, which constitutes a form of gliosis known as microgliosis, begins within hours of the initial CNS injury. Later, after 3–5 days, oligodendrocyte precursor cells are also recruited to the site and may contribute to remyelination. The final component of gliosis is astrogliosis, the proliferation of surrounding astrocytes, which are the main constituents of the glial scar.

Answer 291

Oligodendrocytes

Answer 292

Schwann Cells

Answer 293

Astrocytes

Answer 294

In the periphery, the axon and myelin get degraded & phagocytosed, THEN Schwann cells proliferate!

Answer 295

• Prolactinoma in anterior pituitary

Answer 296

There was no answer to pastefor this -- Jas

Answer 297

* Ku - Vagus elevation of palate (10) * Mi – Facial muscles (7) * Lah – Hypoglossal tongue (12)

Answer 298

• Damage to pallidus, putamen, or thalamus

Answer 299

Damage to anterior region of PCA, which infarcts the splenium of the corpus callosum and does not allow visual information to come across from right to left language area

Answer 300

1) Metastases (generally at the junction of grey and while matter) 2) Astrocytomas (Glioblastoma) 3) Meningioma 4) Pituitary Tumor

Answer 301

1) Poliocytic astrocytoma 2) Medulloblastoma

Answer 302

Craniopharyngioma, arises from EPITHELIAL cells derived from Rathke’s pouch

Answer 303

Temporal lobes and base of frontal lobes

Answer 304

Increased sensitivity to sound; Paralysis of the stapedius, such as in injury to the facial nerve (CN VII), allows wider oscillation of the stapes, resulting in heightened reaction of the auditory ossicles to sound vibration. This condition, known as hyperacusis, causes normal sounds to be perceived as very loud.

Answer 305

Foramen Spinosum in middle cranial fossa

Answer 306

Follicular Epithelial Cells

9/20/2013 Flashcards

(349 cards)