Final Flashcards
What does a lesion of the basal ganglia cause?
Disturbances in the initiation and cessation of movement & motor planning
Corpus Striatum
Caudate nucleus, putamen, globus pallidus (putamen + globus = lenticular nucleus)
What does the basal ganglia consist of?
Corpus striatum, subthalamic nucleus, substantia nigra (internal capsule is a related area)
Destructive lesion of/overactive caudate nucleus
Huntington’s disease, apathy
OCD
Putamen
Relay station between caudate and globus pallidus
Globus Pallidus
Principle source of efferent fibers coming from the corpus striatum
Pathway of the basal ganglia
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)
Dyskinesias
Disorders of cessation/initiation of movement.
Chorea
Rapid, jerky involuntary movements
Athetosis
a continuous series of spontaneous movements that blend into each other
Dystonia
joints locked into place
Hemiballismus
Violent involuntary movement of a limb d/t lesion in CL subthalamic nucleus
Tics
repeated involuntary movements. (tourette’s)
Tics
repeated involuntary movements. (tourette’s)
Huntington’s Disease
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
Choreic (classical) form of Huntington’s
Most common
Adult form of Huntington’s disease
Characterized by: involuntary movements, emotional disturbances, dementia, choreic movements usually decreased w/ sleeping.
Westphal form of Huntington’s
Adult form. characterized by rigidity, choreic movements increase when sleeping
Parkinson’s Disease I
Loss of dopaminergic neurons in substantia nigra and ventral tegmental area (in midbrain) –> loss of control to motor cortex
Parkinson’s Disease II
Loss of cholinergic neurons in pedunculopontine nuclei (located in pons and midbrain) –> excessive activity in the reticulo and vestibulospinal tracts, difficulty w/ gait initiation
3 general types of Parkinson’s
Akinetic/rigid predominant, tremor predominant, mixed
Cardinal signs of Parkinson’s
Tremor, bradykinesia
Cardinal signs of Parkinson’s
Tremor (occurs at rest), bradykinesia, rigidity (lead pipe, cohwheel), postural instability (fall risk)
What are Parkinson’s Signs/Sx due to
a loss of dopaminergic neurons and localized cholinergic neurons
Etiology of PD
most cases have no known cause. multifactorial probably. Environmental, genetics, age.
Parkinson Plus Syndromes
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
Multiple System Atrophy (MSA) P
predominant parkinson’s signs/Sx, striational degeneration, may also have Alzheimers Signs/Sx
MSA C
Predominant cerebellar signs (ataxia) - olivopontocerebellar atrophy
MSA A
predominant ANS signs/Sx. Shy-Drager Syndrome
Progressive Supranuclear palsy (PSP)
Inability to move the eyes up or down, loss of balance, swallowing and speech problems
Corticobasalar ganglion degeneration (CBGD)
Signs/Sx initially on one side, may include alien hand syndrome (uncontrolled hand movement to external stimuli)
What produces CSF?
choroid plexi mainly.
Pathway of CSF
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
Non-Communicating Hydrocephalus
blockage in the ventricles, foramen, aqueduct, apertures, cant travel to subarachnoid space
Communicating Hydrocephalus
blockage in subarachnoid space (arachnoid villi), CSF cant enter the dural venous sinuses
Normal Pressure Hydrocephalus
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
Normal Pressure Hydrocephalus
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
Meningitis
inflammation may block CSF circulation –> hydrocephalus
headaches, altered consciousness, nuchal agitation, labile
encephalitis
Blood vessel diameter dependent on
[O2] & [CO2] vs neural control
↓ [O2] and/or ↑ [CO2] dilates blood vessels
Branches of carotid artery
Middle cerebral, anterior cerebral, posterior communicating.
Middle cerebral artery supplies
motor/sensory to CL face/UE, Broca’s, posterior limb of internal capsule, corpus striatum, optic tract
Anterior cerebral Artery supplies
motor/sensory to CL/LE’s (paracentral lobule), corpus striatum, medial aspects of frontal and parietal lobes, corpus callosum and fornix
Posterior communicating artery
connects internal carotid to PCA, frequent site of aneurysm
Aneurysm
dilation of blood vessel, can occur at arteriovenous malformations
Vertebral arteries
off of subclavian –> transverse foramen of upper 6 cervical vertebrae
braches - A/P spinal, PICA, Basalar, posterior cerebral
Anterior spinal artery supplies
pyramids, hypoglossal nerve, medial lemniscus, ventral and lateral funiculi, ventral gray horn.
Posterior Spinal Arteries
Supply dorsal funiculi
Posterior Spinal Arteries
Supply dorsal funiculi
Posterior inferior cerebellar arteries supplies
Posterior aspects of cerebellum (deep cerebelalr nuclei), dorsal lateral region of medulla (Wallenberg syndrome)
Wallenberg (lateral medullary) Syndrome
“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)
Branches of Basilar artery
SCA, Labrynthian, pontine, AICA
“Locked-In Syndrome”
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.
Posterior cerebral arteries supply
occipital cortex, midbrain
Circle of WIllis
anterior communicating artery, ACA’s, ICA’s, Post. comm. art., PCA’s (potential alternative route if blockage occurs in major branch)
External cerebral veins
Superior cerebral veins – bridging veins
Internal cerebral veins
Great cerebral vein of Galen→straight sinus
Sinuses
Superior sagittal sinus, inferior sagittal sinus→ straight sinus→ transverse sinus→sigmoid sinus
Bridging veins
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
Blood Brain Barrier
Tight junctions between endothelial cells of capillaries, foot processes of astrocytes that surround capillaries
Circumventricular Organs
Areas that lack BBB - basal hypothalamus, pineal gland, area prostrema in 4th venticle
Limbic System
Hippocampal formation, cingulate gyrus, amygdala ,septal area, mammillary bodies, dorsomedian nucleus of the thalamus, anterior nucleus of thalamus
M.O.V.E
Memory, olfaction, Visceral, Emotion
Hippocampal formation
Hippocampus, dentate gyrus, subiculum
Location of Hippocampus
Floor of inferior horn of lateral ventricle within the parahippocampal grus
Function of Hippocampus
Memory
Working memory
short term goal - relevant information
Procedural memory
learned skills - riding bike, language
Declarative memory
facts stored for conscious recall
Amygdala
Emotional - regulate sexual behavior, food & water intake, emotional aspects to sensory stimuli, Fear, frustration, anger, rage, violence
Hippocampal formation is involved in
converting short term memory into long term memory = consolidation
Afferent/Efferent information into hippocampal formation
A: Entorhinal formation, fornix, substantia innominata
E: fornix
Substantia innominata
basal nucleus of Meynert, diagonal band, septal area. Releach AcH degeneration of neurons here implicated in Alzheimers (memory loss).
Which cranial nerves does the limbic system affect?
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)
Pathologies of the limbic system
Kulver-Bucy syndrome, Pick’s disease, Alzheimers
Kulver-Bucy syndrome
Damage to temporal lobes - decreased visual perception, flattened emotions no fear response, increased interest in sex
What causes Pick’s disease
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)
Differences between Picks disease and Alzheimers
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)
Alzheimers disease
Most common cause of dementia
Hallmark neuropathological features of AD
neurofibrillary changes, senile plaque (containing beta amyloid plaque), neuronal loss in hippocampus, substantia nigra, entorhinal cortex and cerebral cortex.
Clinical features of AD
short term memory loss, word finding problems, geographical disorientation, changes in personality, depression.
Causes of Alzheimers
Genetics, Cholinergic hypothesis, Tau hypothesis, oxidative stress hypothesis, beta-amyloid plaque hypothesis
Stage I of AD
Early or mild - mild anterograde amnesia (recent memory) (keys, parked car, anxious/irritable/apathetic, anomia, decreased vocab)
Stage II of AD
middle or moderate - lose memory of all recent events, restless, sundowning, labile, wandering, incontinence, impaired coordination, reduced ability to perform ADL
Stage III AD
late or severe AD - cannot recognize family members or past events, language significantly reduced, withdrawn, decreased desire to ambulate (loss of declarative and procedural)
Dementia with Lewy Bodies
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
Multi-infarct dementia
“vascular dementia” –> second most common. vascular lesions damage parts of the brain.
Symptoms of Multi-infarct dementia
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
Pre-embryonic stage
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
Embryonic stage (general)
day 15-end of week 8, ectoderm differentiates into the epidermis & nervous system
Fetal stage
End of 8th week-birth, myelination begins
Embryonic stage
2 germ layers - endoderm & ectoderm
Endoderm
hypoblast - linings of respiratory and GI tract
Ectoderm
epiblast - epidermis, mesoderm (CT, muscle, blood cells, bone marrow), nervous system
Nervous system development
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,
Neural crest cells
some ectodermal cells remain separate from neural plate –> form PNS, ANS
Lumen of neural tube
ventricles and central canal
Wall of neural tube
ependymal cells, neuroblasts, glial blasts (astrocytes/oligodendrocytes)
Mesoderm surrounding neural tube
forms meningeal layers
Spinal cord development
Day 26 - tube differentiates into mantle layer (inner) Marginal layer (outer)
Mantle layer
becomes gray matter, divides into dorsal section (association/alar plate = dorsal gray matter), ventral section = motor/basal plate (ventral gray horn)
Somites
clusters of mesoderm which develop along neural tube, they divide into sclerotome (vertebrae and skull), dermatome (dermis), myotome (skeletal muscle)
Spina Bifida occulta
Lamina don’t fuse around neural tube defect
Tuft of hair often present over the area
Usually asymptomatic
Spina bifida cystica
cyst that forms
w/ meningocele - meninges protrude through unfused lamina.
w/meningomyelocele - meninges and spinal cord protrude
*variable motor sensory symptoms
Myeloschisis
neural folds fail to fuse
Brain development
4th week - cranial portion of neural tubes forms 3 primary vesicles –> prosencephalon, mesencephalon, rhomencephalon
prosencephalon
Telencephalon (cerebral cortex, subcortical white matter, basal ganglia) Diencephalon (thalamus, hypothalamus, subthalamus, epithalamus, metathalamus)
Mesencephalon
Midbrain
Rhombencephalon
Metencephalon (pons, cerebellum)
Myelencephalon (medulla)
Congenital malformaitons of the brain
anencephaly, hydrocephalus, “growing in”, Arnold-Chiari malformation
“growing in” deficit
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
Arnold-Chiari malformation Types I, II, III, IV
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
Attention deficit hyperactivity disorder (ADHD)
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
Autism
Repetitive behaviors, lack of communication skills, social behavior deficits
Abnormal shapes of caudate, amygdala and putamen
Asperger’s syndrome
High intellect, poor social skills
Passive development disorder NOS
Similar sxs as above but does not fulfill all criteria
Cerebral Palsy
permanent non-progressive damage to developing brain
Types of CP
Spastic, Dyskinetic/Athetoid (lesion in BG ventrolateral thalamus), Ataxic (cerebellum), Mixed (widespread), Hypotonic (floppy baby)
Spastic CP
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
CP etiology
Prenatal (conception to onset of labor), Natal (onset of labor to delivery), Post natal (delivery to 2-3 y.o.)
Prenatal causes
Mothers with rubella or viral infection
Anoxia secondary to pneumonia, C-R disease, diabetes
Maternal drug/alcohol abuse
Natal causes
Trauma or anoxia during labor (premature babies more at risk for anoxia)
Post natal causes
Encephalitis, meningitis or trauma (MVA, child abuse)
