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38 Cards in this Set

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Neurological Disorders
Primary cause within nervous system unlike most behavioral deficits.
-- Benign: Noncancerous, may grow but do not metastisize. Malignant: leave after growing.
--Almost never arise from neurons (b/c neurons do not grow/divide after becoming neurons)
Neurons are post-mitotic
Cancer can arise from the following supporting cells: Glia, astrocytes, myelin, etc. Or from neural blasts (percursors to nerve cells; neuralblastoma).
Damage can be direct (tumor destroying existing tissue) or indirect (tumor causes pressure on another part of the brain due to size, whether benign or malignant) Beh changes depend on location of tumor.
Astrocytic Tumors: Pathology
Photo: GLIOMA brainstem w/ cerebellum. Astrocytic tumor in middle, not visible in myelin stain b/c tumor arose from astrocytes, not Myelin cells; the rest if the myelin containing cells are stained. (Mor skills; closed cerebral aqueduct: introcranial pressure due to fluid buildup) Also an astrocytic tumor in frontal cortex (planning, coord mov)
Seizure Disorders
Includes epilepsy, others (seizures can occur for a variety of reasons).
Partial vs. generalized seizure
Definite focus vs. widespread.
-Uncontrolled electrical event (high amplitude of firing, spreads to other neurons).
Causes unknown
Imbalance between excitation and inhibition in brain (no feedback to prevent seizures) Ranging beh effects also heart rate and resp. Low GABAergic blocking leads to seizures in common seizure areas/eplieptogenic (low levels of gabaergic innervation, small disturbances thereof such as blocking even in low levels lead to seizures).
Seizure Disorders
May relate to NMDA receptors (**ionotr rec frum glu NTs**).
Decreased glucose metabolism in seizure focus PET Scan (radioactive glucose into bloodstream (dec glu metabolism); where being metabolized. Ex. HM: bilateral (deficiencies in glucose metabolism) vs just right side
Seizure Disorders
(*Temporal lobe: dec gabaergic innervation; *Most often involved in seizures. Damage to neural activity vs gross anatomy; living cells except prone to hyperactivity. Arrows show dec glu metabolism (blue/cooler colors)
-Usu spreads to entire brain vs only having seizures to one side of body; can involve entire body. Ex. not currently having a seizure for PET scan diag; normal functioning.
Cerebrovascular Accidents
-Hemorrhagic stroke
-Obstructive stroke
-Hemorrhagic stroke: bleeding at a brain site. Nowhere for blood to go; buildup; growing; influencing surrounding tissue. Should be providing O2 to other cells which will die.
Obstructive stroke
Thrombus—blood clot formed at stroke site; more and more platlets sticking. Prevents blood from getting to other areas/cells.
-Embolus—blood clot travels through vessels (ex. going to brain, starts as thrombosis, when mobilized becomes embollus) Can happen on long plane rides. A deep veinus thormbosis starts in deep veins of legs and then detaches from site of origin and travels through body; tiny capillaries in brain that a big DVT can block easily - obstructive stroke caused by an embollism (becomes an embollus once mobilized).
Explosion of blood vessels or breaking through. Like a hemoragic stroke (general term) but as a specific reason for bleeding (more specific); disease condition causing blood walls to thin and maybe high blood pressure.
Can (usu) occur in dura, arachnoid (middle) or pia (pads covering brain; subdural hematomas, aneurysm betwn dura and arachnoid. (Sudden, acute) Usu very dangerous bc cause instant inc in cerebral pressure causing it to stop func.
Hemorrhagic Stroke: Pathology
Pic one: Hemorrhage-main effect on motor cortex and caudate. Hemoorhagic stroke; bv started bleeding in brain under motor cortex. Not a hole in brain but red blood cells; infiltrating spaces btwn neurons/glia. Loose motor func on left side (if on right side of brain)
Pic two: Hemorrhage-main effect on parietal cortex
(Reduced magnitude) Can cause fissures vs gyri (would rather distintegrate or explode) to unfold. Pic 3: obstructive stroke caused by embolism.
(No warning signs; can occur over hours; aspirin: blood thinner helps w/ obstructive strokes vs hemorrhagic (for ex. may start w/ slurred speech, etc) But if you have an aneurysm and take a blood thinner you would bleed more and clot less. (Smoking while on the pill further thins blood vessels.)
Disorders Associated with Dopamine
Parkinson’s Disease
--Parkinson’s Disease
Caused by a loss of dopaminergic cells in the substantia nigra.
In US the most common neurodegeneratic disorder.
Unknown cause of loss of cells. Affects the nigrostriatal pathway (loss of cells, affects pathway) (Bundle of nuclei assoc w/ motor func)
Promising area of stem cell research. (Produce dopamine, implant in substa nigra, reinnervate parts of brain where these cells being lost originally innervate. At least a slowing in progression of disease.
Parkinson’s Disease: Pathology
Much less dopamine producing cells in substantia nigra with parkinson's disease. (10-15% of normal amount)
Parkinson’s Disease
**Affects are due to imbalance in the motor-control circuit
[(Originates in Motor cortices) Parietal-(sub nigra sends info to and usu inhibits) striatum (projects to thalamus and motor cortex)]
Causes motor deficits (walking, posture); affects are due to an imbalance in the motor control circuit (no longer regulated). - Signal originates in pre-motor corticies -> Parietal cortex (does not project directly to motor cortex); sends info through striatum which receives info from sub nigra. Sub nigra ordinarily inhibits func of striatal cells (which project to thalamus and motor cortex)(delicately). Ex. over/under controlled movement. Without sub nigra: loose fine motor control. (Easier for partietal cortex signal to get through straitum and into thalamus and motor cortex) Ex. resting tremor - parietal cortex says to move and not inhibited. Usu ongoing inhibition, below activational level, to stay still.
A serious mental disorder characterized by disordered thoughts, delusions, hallucinations, and often bizarre behaviors.
Positive symptoms
Evident by their presence: delusions, hallucinations, or thought disorders
Negative symptoms
The absence of behaviors that are normally present:
social withdrawal, lack of affect, and reduced
Age of onset around 20-30 yrs.
Numerous brain regions involved.
(Frontal lobe: critical to problem solving, insight and other high-level reasoning; perturbations in sch lead to difficulting in planning. Limbic sys: distrubances are thoughts to contribute to the agitation. Basal ganglia: involved in mov and emotions and integrating sensory info; excessive blockade of da rec in basal ganglia by traditional antipsy medications leads to motor side effects. Auditory system (overactivity of speech area/wernicke's; auditory halluc. Occiptal lobe: interpreting emotions, images. Hippocampus (learning and memory func).
Schizophrenia: The dopamine hypothesis
A typical neuroleptic, dopamine receptor blocker
An atypical neuroleptic (neuroletpic: dopamine rec blocker), an antipsychotic drug; late '50s.
Blocks D4 receptors in the nucleus accumbens. [Better drugs blocked dopaminergic rec.]
The Dopamine Hypothesis of Schizophrenia
Normal controls and unmedicated schizophrenics; given amphetamine (causing dopamine release from dopaminergic neurons). Sch showed higher DA rel. (Which inc post symptoms (number, severity, etc)) (Crystal meth may inc conditions similar to sch.)
Schizophrenia: Other hypotheses
[Inc dopamine does not account for neg sym. b/c should be improving them like positive symptoms]
-Research suggest several environmental factors:
Season of birth (winter)
Viral epidemics
Population density (more dense, per capita)
Latitude (near equator dec change; increased in N and dec in S)
Prenatal malnutrition
Rh incompatibility (blood type; (ex. esp if you are pos and mother neg) w/ mother)
Maternal stress
Schizophrenia: Degenerative?
(Left parietal cortex area, speech, not lost -> positive symptoms emerging)
Increased amount of brain for empty space (ventricle size). (Gray matter usu increases in adolescence but in sch the cortex dec)
- Correlates w/ dec gray matter in sch. (Avg annual loss). Even worse 5 yrs later (up to 20% deficit, no region essentially spared/ Speech areas not degen - overpowers area keeping it in check before. Barely any regions spared.
Alzheimer’s Disease
Progressive neurodegenerative disease
No known single cause
Affected 4.5 Million people in 2004; More than doubled since 1980
Likelihood of developing Alzheimer’s disease doubles every 5 years after age 65
By the age of 85, risk is about 50%
Affects memory, speech, some motor function. Normally there is no space btwn gyri; much space in sch. Loss of cortical tissue; gray matter.
Alzheimer’s Disease Pathology
tangles (two features indicating diesease; nervous tissues)
Multiple Sclerosis
Progressive loss of myelin
Thought to be an autoimmune disorder
Patient’s own immune system attacks the myelin sheath
Symptoms include motor defecits, fatigue, pain, numbness (“pins and needles”)
Variable disease course
(Maybe stable for a few yrs)
Multiple Sclerosis: Pathology
Loss of white matter and myelin (diag).
Amyotrophic Lateral Sclerosis
((ALS: Pathology))
ALS, Lou Gherig’s Disease
(Also Stephen Hawking) Progressive neurodegenerative disease
Loss of motor neurons in the spinal cord and brain
Paralysis of distal extremities first, move proximal with varying rates, ultimately leads to paralysis of nerves controling diaphragm
Huntington’s Disease
Neurodegenerative disease
Affects the caudate nucleus
Characterized by motor deficits
“Huntington’s Chorea” (dance)
Along with metastases, are the most serious types of tumors. Derived from glial cells; very malignant and fast growing. --A benign brain tumor composed of the cell that constitute the meninges (dura mater or arachnoid)
Seizures (most do not involve the motor sys: convulsions)
Partial: typically a scarred region caused by an old injury. Simple partial: changes in consciousness but not loss. Complex: loss of consc due to location/severity.
Most severe form of seizure: grand mal:
--Tonic phase:
Generalized; often includes motor sys of brain. --A few seconds before seizure occurs; caused by excitation of neurons surroundng a seizure focus. --Begining of a grand mal seizure; muscles contract; invol cry; then hold posture.
--Clonic phase:
--Absence spells
--Status epilepticus
Agitated; jerking; eyes rolling; contortions. Then sleep. --Children usu; generalized; petit mal. --Series of seizures w/o regaining consc. (Excess rel of glu during seizure)
NMDA receptors and seizures caused by alcohol withdrawal
(Specialized glu rec controlling ca ch which open only when glu binds and mem is depol) Alcohol blocks nmda rec.
Hemorrahgic strokes
--Free radicals
Bleeding w/in brain usu from malformed bv or bvs weakened by high bp. Obstructive strokes can be caused by thrombi or emboli. (Excessive glu vs loss of o2...) --Molecules w/ unpaired electrons that act as powerful oxidizing agends; toxic to nuc acids, proteins, fatty acids. Drugs now to inactivate free radicals.
Degen of nigrostriatal- the DA sec neurons of sub nigra that send axons to the basal ganglia. --Many surving DA neurons show Lewy bodies, abnormal circular structures found w/in cytoplasm; have a dense protein core surrounded by a halo of radiating fibres. Most cases do not have genetic orgins, but a mutation of a gene located on chromosome 4 will produce disorder by producing a protein known as alpha-synuclein.
--Parkin mutated gene whch produces proteins which ferry defective proteins to the proteosomes to destroy them.
Normally found in presyn mem, where it is apparently involved in synaptic plasticity. Abnormal accumulations cause neural degen. Dense core of Lewy bodies consists of these aggregations. --Permits toxic levels of alpha-syn to accumulate in DA neurons.
Internal division of globus pallidus (GPi)
Division of GP that provides inhib input to the motor cortex via the thalamus; sometimes stereotaxically lesioned to treat symptoms.
Huntington's disease:
No treatment; future role of faulty hungingtin protein.
Also a basal ganglia diesease caused by the degen of the caudate nuc and putamen (first sign of neural degen thereof which should be inhib), esp of gabaergic and acetyl neurons. Not poverty of mov but uncontrollable ones. Fatal; usu begins in 30-40s.
Severe degen of Hippocampus, entorhinal cortex, neocortex, nuc basalis, locus coeruleus, raphe nuc (HEN NucBLR)
As in down syndrome, develop Neuritic plaques and neurofibirillary tangles.
Neuritic: extracellular deposits w/ Beta-amyloid, surrounded by degenerating axons and dendrites and activated microglia and reactive astrocytes. Only core left later.
neurofibirillary tangles
Intraceullar; dying neurons that contain intracellular accumulations of twisted filaments of tau protein (component of microtubules for transport). Abnormal filaments disrupt transport w/in cell and the cell dies leaving a tangle of protein filaments.
Emotion: Lateral Nuc
(Orbitofrontal cortex)
Receives sensory info from primary sensory cortex, assoc cortex, thalamus, and hippocampal formation. Along with Basal and Accessory Basal Nuclei, sends info to CE (central nucleus) which projects to hypothal, midbrain, pons, medulla. CE: Single most important for emotions by aversive stimuli; increased activity and fos protein. --Base of anterior frontal lobes; prefrontal cortex region; control of emotion.