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Neuroanatomy > Final > Flashcards

Final Flashcards

1
Q

What does a lesion of the basal ganglia cause?

A

Disturbances in the initiation and cessation of movement & motor planning

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2
Q

Corpus Striatum

A

Caudate nucleus, putamen, globus pallidus (putamen + globus = lenticular nucleus)

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3
Q

What does the basal ganglia consist of?

A

Corpus striatum, subthalamic nucleus, substantia nigra (internal capsule is a related area)

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4
Q

Destructive lesion of/overactive caudate nucleus

A

Huntington’s disease, apathy

OCD

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5
Q

Putamen

A

Relay station between caudate and globus pallidus

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6
Q

Globus Pallidus

A

Principle source of efferent fibers coming from the corpus striatum

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7
Q

Pathway of the basal ganglia

A

motor and sensory cortex, substantia nigra, and subthalamic nuclei send input into the basal ganglia (skeletal motor loop) –> basal ganglia indirectly affect spinal cord motor neurons by influencing activity of neurons in the pre-motor and primary motor areas (corticospinal tract)

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8
Q

Dyskinesias

A

Disorders of cessation/initiation of movement.

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9
Q

Chorea

A

Rapid, jerky involuntary movements

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10
Q

Athetosis

A

a continuous series of spontaneous movements that blend into each other

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11
Q

Dystonia

A

joints locked into place

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12
Q

Hemiballismus

A

Violent involuntary movement of a limb d/t lesion in CL subthalamic nucleus

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13
Q

Tics

A

repeated involuntary movements. (tourette’s)

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14
Q

Tics

A

repeated involuntary movements. (tourette’s)

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15
Q

Huntington’s Disease

A

Genetically transmitted, causes dementia and choreiform movements, defect on chromosome 4 (produces a mutated from of a protein that aggregates in the basal ganglia and causes atrophy of putamen and caudate)
characterized by excessive inhibition of the output nuclei of BG –> release inhibition of motor thalamus –> uncontrolled motor output

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16
Q

Choreic (classical) form of Huntington’s

A

Most common
Adult form of Huntington’s disease
Characterized by: involuntary movements, emotional disturbances, dementia, choreic movements usually decreased w/ sleeping.

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17
Q

Westphal form of Huntington’s

A

Adult form. characterized by rigidity, choreic movements increase when sleeping

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18
Q

Parkinson’s Disease I

A

Loss of dopaminergic neurons in substantia nigra and ventral tegmental area (in midbrain) –> loss of control to motor cortex

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19
Q

Parkinson’s Disease II

A

Loss of cholinergic neurons in pedunculopontine nuclei (located in pons and midbrain) –> excessive activity in the reticulo and vestibulospinal tracts, difficulty w/ gait initiation

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20
Q

3 general types of Parkinson’s

A

Akinetic/rigid predominant, tremor predominant, mixed

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21
Q

Cardinal signs of Parkinson’s

A

Tremor, bradykinesia

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22
Q

Cardinal signs of Parkinson’s

A

Tremor (occurs at rest), bradykinesia, rigidity (lead pipe, cohwheel), postural instability (fall risk)

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23
Q

What are Parkinson’s Signs/Sx due to

A

a loss of dopaminergic neurons and localized cholinergic neurons

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24
Q

Etiology of PD

A

most cases have no known cause. multifactorial probably. Environmental, genetics, age.

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25
Q

Parkinson Plus Syndromes

A

A group of neurodegenerative diseases that exhibit the classical features of Parkinson’s disease with additional sxs/signs not strongly associated with Parkinson’s disease

These syndromes are usually more rapidly progressive than PD, and are less likely to respond to medications used for PD

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26
Q

Multiple System Atrophy (MSA) P

A

predominant parkinson’s signs/Sx, striational degeneration, may also have Alzheimers Signs/Sx

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27
Q

MSA C

A

Predominant cerebellar signs (ataxia) - olivopontocerebellar atrophy

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28
Q

MSA A

A

predominant ANS signs/Sx. Shy-Drager Syndrome

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29
Q

Progressive Supranuclear palsy (PSP)

A

Inability to move the eyes up or down, loss of balance, swallowing and speech problems

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30
Q

Corticobasalar ganglion degeneration (CBGD)

A

Signs/Sx initially on one side, may include alien hand syndrome (uncontrolled hand movement to external stimuli)

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31
Q

What produces CSF?

A

choroid plexi mainly.

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32
Q

Pathway of CSF

A

lateral ventricle –> foramen of monroe –> 3rd vent –> aqueduct –> 4th ventricle –>median/lateral apertures –> subarachnoid space and central canal –> reabsorbed by arachnoid villi –> venous sinuses –> venous circulation

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33
Q

Non-Communicating Hydrocephalus

A

blockage in the ventricles, foramen, aqueduct, apertures, cant travel to subarachnoid space

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34
Q

Communicating Hydrocephalus

A

blockage in subarachnoid space (arachnoid villi), CSF cant enter the dural venous sinuses

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35
Q

Normal Pressure Hydrocephalus

A

Type of non-communicating. CSF pressure increased, ventricles expand so now pressure is normalized but brain damage has occurred.
Sx: ataxic gait (damage to corticospinal fibers in internal capsule), urinary incontinece, dementia.
Wet, Wobbly, Weird

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36
Q

Normal Pressure Hydrocephalus

A

Type of non-communicating. CSF pressure increased, ventricles expand so now pressure is normalized but brain damage has occurred.
Sx: ataxic gait (damage to corticospinal fibers in internal capsule), urinary incontinece, dementia.
Wet, Wobbly, Weird

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37
Q

Meningitis

A

inflammation may block CSF circulation –> hydrocephalus
headaches, altered consciousness, nuchal agitation, labile
encephalitis

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38
Q

Blood vessel diameter dependent on

A

[O2] & [CO2] vs neural control

↓ [O2] and/or ↑ [CO2] dilates blood vessels

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39
Q

Branches of carotid artery

A

Middle cerebral, anterior cerebral, posterior communicating.

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40
Q

Middle cerebral artery supplies

A

motor/sensory to CL face/UE, Broca’s, posterior limb of internal capsule, corpus striatum, optic tract

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41
Q

Anterior cerebral Artery supplies

A

motor/sensory to CL/LE’s (paracentral lobule), corpus striatum, medial aspects of frontal and parietal lobes, corpus callosum and fornix

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42
Q

Posterior communicating artery

A

connects internal carotid to PCA, frequent site of aneurysm

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43
Q

Aneurysm

A

dilation of blood vessel, can occur at arteriovenous malformations

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44
Q

Vertebral arteries

A

off of subclavian –> transverse foramen of upper 6 cervical vertebrae
braches - A/P spinal, PICA, Basalar, posterior cerebral

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45
Q

Anterior spinal artery supplies

A

pyramids, hypoglossal nerve, medial lemniscus, ventral and lateral funiculi, ventral gray horn.

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46
Q

Posterior Spinal Arteries

A

Supply dorsal funiculi

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47
Q

Posterior Spinal Arteries

A

Supply dorsal funiculi

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48
Q

Posterior inferior cerebellar arteries supplies

A

Posterior aspects of cerebellum (deep cerebelalr nuclei), dorsal lateral region of medulla (Wallenberg syndrome)

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49
Q

Wallenberg (lateral medullary) Syndrome

A

“Crossed analgesia” IL loss of pain/temp in face (damage to spinal trigeminal tract), CL loss pain/temp to limbs/trunk (damage to spinothalamic tract), Ataxia (damage to ICP), dysarthria/dysphagia (damage to ambuguus nucleus), horners syndrome (damage to descending sym. tract)

50
Q

Branches of Basilar artery

A

SCA, Labrynthian, pontine, AICA

51
Q

“Locked-In Syndrome”

A

Complete basalar artery thrombosis w/ bilateral infarction of the pons, quadriplegia, impairment of function of CN’s V, mutism Preserved - consciousness, blinking and vertical eye movements.

52
Q

Posterior cerebral arteries supply

A

occipital cortex, midbrain

53
Q

Circle of WIllis

A

anterior communicating artery, ACA’s, ICA’s, Post. comm. art., PCA’s (potential alternative route if blockage occurs in major branch)

54
Q

External cerebral veins

A

Superior cerebral veins – bridging veins

55
Q

Internal cerebral veins

A

Great cerebral vein of Galen→straight sinus

56
Q

Sinuses

A

Superior sagittal sinus, inferior sagittal sinus→ straight sinus→ transverse sinus→sigmoid sinus

57
Q

Bridging veins

A

Branches off superior cerebral veins → across subarachnoid space → through arachnoid membrane → across subdural space → through dura mater → superior sagittal sinus

Rupture of vessel:
Subarachnoid or subdural hemmorhage

58
Q

Blood Brain Barrier

A

Tight junctions between endothelial cells of capillaries, foot processes of astrocytes that surround capillaries

59
Q

Circumventricular Organs

A

Areas that lack BBB - basal hypothalamus, pineal gland, area prostrema in 4th venticle

60
Q

Limbic System

A

Hippocampal formation, cingulate gyrus, amygdala ,septal area, mammillary bodies, dorsomedian nucleus of the thalamus, anterior nucleus of thalamus

61
Q

M.O.V.E

A

Memory, olfaction, Visceral, Emotion

62
Q

Hippocampal formation

A

Hippocampus, dentate gyrus, subiculum

63
Q

Location of Hippocampus

A

Floor of inferior horn of lateral ventricle within the parahippocampal grus

64
Q

Function of Hippocampus

A

Memory

65
Q

Working memory

A

short term goal - relevant information

66
Q

Procedural memory

A

learned skills - riding bike, language

67
Q

Declarative memory

A

facts stored for conscious recall

68
Q

Amygdala

A

Emotional - regulate sexual behavior, food & water intake, emotional aspects to sensory stimuli, Fear, frustration, anger, rage, violence

69
Q

Hippocampal formation is involved in

A

converting short term memory into long term memory = consolidation

70
Q

Afferent/Efferent information into hippocampal formation

A

A: Entorhinal formation, fornix, substantia innominata
E: fornix

71
Q

Substantia innominata

A

basal nucleus of Meynert, diagonal band, septal area. Releach AcH degeneration of neurons here implicated in Alzheimers (memory loss).

72
Q

Which cranial nerves does the limbic system affect?

A 
CN VII (lacrimal salivary, facial)
CN III , IV, VI,  (movements toward or away from visual sites)
CN X (GI tract responses to visual or olfactory sensations, HR)
73
Q

Pathologies of the limbic system

A

Kulver-Bucy syndrome, Pick’s disease, Alzheimers

74
Q

Kulver-Bucy syndrome

A

Damage to temporal lobes - decreased visual perception, flattened emotions no fear response, increased interest in sex

75
Q

What causes Pick’s disease

A

large aggregations of proteins in neurons of frontal and temporal lobes resulting in neuronal death and atrophy in these areas (one cause of frontal-temporal lobar degeneration)

76
Q

Differences between Picks disease and Alzheimers

A

earliest symptoms are behavioral changes (vs. memory loss) d/t involement of prefrontal cortex. Impulsivity, obsessive/compulsive, drinking/eating to excess, lack of attention to personal hygeine, poor judgement, sexual exhibitionism/promiscuity)

77
Q

Alzheimers disease

A

Most common cause of dementia

78
Q

Hallmark neuropathological features of AD

A

neurofibrillary changes, senile plaque (containing beta amyloid plaque), neuronal loss in hippocampus, substantia nigra, entorhinal cortex and cerebral cortex.

79
Q

Clinical features of AD

A

short term memory loss, word finding problems, geographical disorientation, changes in personality, depression.

80
Q

Causes of Alzheimers

A

Genetics, Cholinergic hypothesis, Tau hypothesis, oxidative stress hypothesis, beta-amyloid plaque hypothesis

81
Q

Stage I of AD

A

Early or mild - mild anterograde amnesia (recent memory) (keys, parked car, anxious/irritable/apathetic, anomia, decreased vocab)

82
Q

Stage II of AD

A

middle or moderate - lose memory of all recent events, restless, sundowning, labile, wandering, incontinence, impaired coordination, reduced ability to perform ADL

83
Q

Stage III AD

A

late or severe AD - cannot recognize family members or past events, language significantly reduced, withdrawn, decreased desire to ambulate (loss of declarative and procedural)

84
Q

Dementia with Lewy Bodies

A

cognitive decline of executive functions, vivid dreams/hallucinations, Signs/Sx vary day to day, similar to AD b/c bodies destroy cholinergic and dopaminergic neurons, accumulations of cell protein called alpha synuclein

85
Q

Multi-infarct dementia

A

“vascular dementia” –> second most common. vascular lesions damage parts of the brain.

86
Q

Symptoms of Multi-infarct dementia

A

Gradual onset of cognitive impairment following a stroke (memory, decreased ability to follow directions)
Apathy and abulia (lack of will)
Emotional lability
Rapid, shuffling gait
Incontinence
Have episodes of improved memory which somewhat distinguishes it from AD
RIsks - smoking, HTN, CVD, high cholesterol

87
Q

Pre-embryonic stage

A

Conception to day 14 –> fertilized ovum divides as it travels down the uterine tube to uterus, inner cell mass forms consisting of endoderm and ectoderm layers

88
Q

Embryonic stage (general)

A

day 15-end of week 8, ectoderm differentiates into the epidermis & nervous system

89
Q

Fetal stage

A

End of 8th week-birth, myelination begins

90
Q

Embryonic stage

A

2 germ layers - endoderm & ectoderm

91
Q

Endoderm

A

hypoblast - linings of respiratory and GI tract

92
Q

Ectoderm

A

epiblast - epidermis, mesoderm (CT, muscle, blood cells, bone marrow), nervous system

93
Q

Nervous system development

A

ectodermal cells form primitive streak –> forms notochord –> induces ectoderm to form neural plate (day 16) –> neural tube (day 21 - forms CNS), cranial end closed by day 27 (anencephaly if it doesn’t), caudal closes by day 30,

94
Q

Neural crest cells

A

some ectodermal cells remain separate from neural plate –> form PNS, ANS

95
Q

Lumen of neural tube

A

ventricles and central canal

96
Q

Wall of neural tube

A

ependymal cells, neuroblasts, glial blasts (astrocytes/oligodendrocytes)

97
Q

Mesoderm surrounding neural tube

A

forms meningeal layers

98
Q

Spinal cord development

A 
Day 26 - tube differentiates into mantle layer (inner) 
Marginal layer (outer)
99
Q

Mantle layer

A

becomes gray matter, divides into dorsal section (association/alar plate = dorsal gray matter), ventral section = motor/basal plate (ventral gray horn)

100
Q

Somites

A

clusters of mesoderm which develop along neural tube, they divide into sclerotome (vertebrae and skull), dermatome (dermis), myotome (skeletal muscle)

101
Q

Spina Bifida occulta

A

Lamina don’t fuse around neural tube defect
Tuft of hair often present over the area
Usually asymptomatic

102
Q

Spina bifida cystica

A

cyst that forms
w/ meningocele - meninges protrude through unfused lamina.
w/meningomyelocele - meninges and spinal cord protrude
*variable motor sensory symptoms

103
Q

Myeloschisis

A

neural folds fail to fuse

104
Q

Brain development

A

4th week - cranial portion of neural tubes forms 3 primary vesicles –> prosencephalon, mesencephalon, rhomencephalon

105
Q

prosencephalon

A

Telencephalon (cerebral cortex, subcortical white matter, basal ganglia) Diencephalon (thalamus, hypothalamus, subthalamus, epithalamus, metathalamus)

106
Q

Mesencephalon

A

Midbrain

107
Q

Rhombencephalon

A

Metencephalon (pons, cerebellum)

Myelencephalon (medulla)

108
Q

Congenital malformaitons of the brain

A

anencephaly, hydrocephalus, “growing in”, Arnold-Chiari malformation

109
Q

“growing in” deficit

A

Neurons with long axons must be fully myelinated before they are fully functional
Process begins in 4th fetal month & ends at end of age 3
Functional deficits d/t impaired myelination would not be obvious until > age 2

110
Q

Arnold-Chiari malformation Types I, II, III, IV

A

Varying degrees of brainstem and cerebellum (tonsils) protrusion through the foramen magnum due to maldevelopment of the posterior cranial fossa
Symptoms vary with severity of damage to neural structures
Headaches due to disruption of CSF flow, weakness, vertigo, nausea

111
Q

Attention deficit hyperactivity disorder (ADHD)

A

Inappropriate inattention, impulsivity and motor restlessness
Childhood ADHD persists into adulthood in 15%-65% of cases
Reduced volume found in frontal cortex, caudate, putamen, cingulate gyrus and cerebellum

112
Q

Autism

A

Repetitive behaviors, lack of communication skills, social behavior deficits
Abnormal shapes of caudate, amygdala and putamen

113
Q

Asperger’s syndrome

A

High intellect, poor social skills

114
Q

Passive development disorder NOS

A

Similar sxs as above but does not fulfill all criteria

115
Q

Cerebral Palsy

A

permanent non-progressive damage to developing brain

116
Q

Types of CP

A

Spastic, Dyskinetic/Athetoid (lesion in BG ventrolateral thalamus), Ataxic (cerebellum), Mixed (widespread), Hypotonic (floppy baby)

117
Q

Spastic CP

A

Spastic (65%) (d/t cocontraction, hyperreflexia, UMN overactivity)
Lesion in cerebral cortex, corticospinal and corticobulbar tracts

Damage to corticospinal tracts during development reduces the normal competition for synaptic sites → inappropriate connections persist → cocontraction

Damage to corticobulbar tracts → disinhibition of spinal reflexes (hyperreflexia) and disinhibition of reticulospinal/vestibulospinal tracts → UMN overactivity

118
Q

CP etiology

A

Prenatal (conception to onset of labor), Natal (onset of labor to delivery), Post natal (delivery to 2-3 y.o.)

119
Q

Prenatal causes

A

Mothers with rubella or viral infection
Anoxia secondary to pneumonia, C-R disease, diabetes
Maternal drug/alcohol abuse

120
Q

Natal causes

A

Trauma or anoxia during labor (premature babies more at risk for anoxia)

121
Q

Post natal causes

A

Encephalitis, meningitis or trauma (MVA, child abuse)

Neuroanatomy (9 decks)

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