THE PARIETAL LOBES: Process and integrate somatosensory and visual information.

Anatomy of the Parietal lobes:

Anterior border-Central Fissure, Ventral border- Sylvian Fissure, Dorsally by the cingulate gyrus, Posterior border- Parieto,
Occipital Sulcus. Subdivisions of the Parietal Lobe: Postcentral Gyrus: Broadmanns areas 1,2,3, Superior Parietal Lobe:
Broadmanns areas 5 and 7, Parietal Operculum: Broadmanns area 43, Supramarginal Gyrus: Broadmanns 40, Angular
Gyrus: Broadmanns area 39. Functional zones: Anterior zone: BA 1,2,3 and 43-Somatosensory cortex. Posterior zone:
remaining areas- posterior parietal cortex. Von Economo: Posterior parietal areas- PE (BA 5 and part of 7). PF (BA 40, 43 and
part of 7). PG- Polymodal (BA39,40). Connections of the Parietal Lobes: Somatosensory strip: To area PE: Tactile
Recognition, To motor regions: sensory information about limb position and movement. Areas PE, PF, and PG: over 100
inputs and outputs exist, 4 Principles of the connections. Area PE is somatosensory: Inputs from the somatosensory strip,
Outputs to primary motor cortex, supplementary motor cortex, premotor regions and area PF, Functions in guiding movement
by providing info about limb position. Area PF: Input form somatosensory (through PE), primary motor cortex and small
visual input through area PG. Outputs to primary motor cortex, supplementary motor cortex , premotor regions. Functions in
guidance of movement. Area PG: Receives complex connections, including visual, somatosensory, proprioceptive, auditory,
vestibular, oculomotor, and cingulate connections. Part of dorsal stream that controls spatially guided behavior with visual
and tactile info. Parietal functional connections: Close relation between the posterior parietal connections and the
prefrontal cortex. Also, both project to the hippocampus. Controls spatially guided behavior. A theory of parietal lobe
function: Anterior zone: Process somatic sensations and perceptions. Posterior zone- (Spatial)- Integrate information
from vision with somatosensory information for movement. Also functions in mental imagery, mental rotation and spatial
navigation. Use of Spatial Information: Object recognition: Viewer centered object recognition: Determines the location,
location orientation and motion of an object, details like color are irrelevant. Object centered: Detail
matters(color,shape,size,spatial relations) Guidence of movement: We transform sensory info into commands for directing
attention and motor ouput. Sensorimotor Transformation: Moving toward an object requires integration and constant
updating of eye, body, limb movements and plans/goals for movement. Area PRR involved in movement.(Can be used in
neuroprosthetics) Spatial Navigation: Cognitive spatial map: Route knowledge plus sense of direction. Medial Parietal
region (MPR) and posterior cingulate gyrus: Neurons show responses associated with making a specific movement at a
specific location. White Matter Organization and Spatial Cognition: Mental transformations are carried out by the
posterior parietal cortex. Noted sex difference in the ability to perform mental transformations of objects. (men outperform
women) Tohmas WOlbers and colleagues used MRI to find relationship between mental relationship proficiency and white
matter organization in the intraparietal sulcus. Men: right parietal lobe, Gesalt strategy(rotate fig as a whole) Women: Right
inferior frontal gyrus, Piecemeal and verbal strategy, count cubes. Other aspects of Parietal Function: Three symptoms
of parietal lobe damage do not fit with the visuomotor view of the parietal lobe. 1. Difficulties with arithmetic, 2.
Difficulties with certain aspects of language, 3. Difficulties with movement sequences. Acalculia: Inability to do arithmetic,
noted in parietal lobe patients, might result from the spatial properties of addition and subtraction. Language: Words have
spatial organization Movement Sequencing: Individual elements of the movement have a spatial organization.
Somatosensory Symptoms of Parietal lobe Lesions: Lesions to the postcentral gyrus produce: Abnormally high
sensory thresholds, Impaired position sense, Astereognosis: Inability to recognize object by tactile perception, Afferent
paresis: Clumsy finger movements due to lack of feedback about finger position. Somatoperceptual Disorders:
Astereognosis: Inability to recognize an object by touch. Asomatognosia: Loss of knowledge or sense of ones own body.
Asymbolia for pain: Absense of normal reactions to pain Anosognosia: Unawareness or denial of illness. Symptoms of
Posterior Parietal Lobe damage: Bailnts Syndrome: cant fixate on a visual stimuli, Neglect of objects, limited field of
attention, Optic Ataxia: deficit in reaching. Contralateral Neglect: Neglect for visual, auditory, and tactile stimulation on
one side of the body or space. Object recognition: After right inferior Parietal lobe lesions patients are poor at recognizing
objects in unfamiliar views. Gerstmann Syndrome: Finger agnosia, Inability to name or recognize fingers, right left
confusion, Agraphia, Acalculia, RESULTS FROM A LEFT PARIETAL LOBE LESION. Other Left Parietal Symptoms: Disturbed
Language function: Agraphia: Inability to write, Dyslexia, Dysphasia: errors on grammar. Apraxia: Movement disorder
in which the loss of movement is not caused by weakness, inability to move, abnormal muscle tone, intellectual deterioration,
poor comprehension or other disorders of movement. Dyscalculia: Difficulties with arithmetic. Poor Recall, Inability to
discriminate left from right. Apraxia and the Parietal Lobe: Ideomotor Apraxia: Cannot copy serial movements or make
gestures, more likely to be associated with left parietal lesions. COnstructural Apraxia: Cannot copy pictures, build puzzles,
or copy a series of facial movements, associated with left and right parietal lesions. Kimura box test Disorders of Spatial
Cognition: Mental Rotation: Left hemisphere deficit may result from the inability to generate the image, Right hemisphere
deficit may result from the inability to manipulate the image. Inability to use topographic information is associated with right
hemisphere change. Major Symptoms and Their Assessment: Somatosensory threshold: 2 point discrimination test.
Tactile Form Recognition, Seguin-Goddard Form Board Test: Blindfolded subject manipulates blocks and attempts to place
them in correct space. Then draw board from memory. Contralateral Neglect: Line Bisection Mark the middle of each of a
set of 20 lines, If neglect, person will typically fail to mark lines on the left side of the page. Visual Perception: Mooney
closure faces test. Gollin incomplete figures test: Subjects shown incomplete faces or objects and must combine
elements to form a whole then identify picture. Spatial Relations: Left-Right discrimination. Language: Token Test.
SPATIAL BEHAVIOR: Spatial Behavior: guides us through space Topographic memory: Ability to move though space
from one place to the next. Cognitive Maps: Mental representaions we have of space. We create maps of the environment
then use hose maps to navigate that environment. Organization of Spatial Behavior: Body space: Surface of the body,
Grasping Space: Area around the body Distal Space: Space the body moves in and out of. Time Space: Past and future,
Awareness of oneself as a continuous entity. Topographic Disorientation : Disability on finding your way around.
Topographic Agnosia: Inability to identify individual landmarks. Topographic amnesia: Inability to remember the
relationship between landmarks. RetroGrade Spatial Amnesia, Anterograde Spatial Amnesia. Brain Regions
Compromised in Spatial Disorientation: Egocentric disorientation: Posterior Parietal, Unable to represent location of

object with respect to self. Heading Disorientation: Right posterior cingulate damage, Unable to set a course, no sense of
direction. Can recognize landmarks. Landmark Agnosia: Right or bilateral lingual, fusiform, parahippocampal gyrus
damage. Unable to use prominent environmental features for orientation. May use detailed features to identify home.
Anterograde Disorientation: Parahippocampal gyrus lesion, Unable to learn representations. Dorsal Stream-Parietal:
Actions toward or away from objects, Egocentric. Dorsal Stream-Frontal: Discrimination tasks which require memory for
spatial location. Pages of visual stimuli, point to one stimulus per page without pointing to same location twice. Dorsal
Stream-Temporal: Spatial Navigation Ventral Stream-Temporal: Complex actions that use objects for references; object
perception. Parceling contribution is not straightforward. Both converge on hippocampus. Integrate ego and allocentric.
Types of Spatial Behavior: Route following: Follow a road or path to a specific object/location. Some animals follow a
light gradient toward or away from light; follow olfactory cues-taxon navigation. Piloting: Ability to find a place that is not
directly marked by a route or cue; place learning. Morris water task (rat maze). Dead Recokoning/Path Integration:
Depends on cues generated by ones own movement; sense of direction. An early form of navigation that uses direction,
speed and travel time. Nonhuman animals- Self movement cues for dead reckoning, sensory flow, movement commands,
hippocampal damage impairs path integration. Single cell recording within the hippocampal formation: Place cells:
disharge at spatial location irrespective of location. Head direction: Discharge when head points in a given direction,
irrespective of location. Grid cells: discharge at many locations forming a virtual grid, possibly maps the size of the
environment. NEUROLOGICAL DISORDERS Vascular Disorders: Cerebral vascular accident: Stroke: the sudden
disruption of blood flow to the brain, Infarct: area of dead or dying tissue resulting from an obstruction of the blood vessels.
Can range from mild to severe. Cerebral Ischemia: Ischemia:Blockage of blood vessels, Thrombosis: Formation of a plug
or clot in the blood vessel. Embolism: A clot or plug that is brought through the blood from vessel to a smaller vessel. Can
be a clot, bubble of air or a mass of cells. Cerebral Ateriosclerosis: Thickening and hardening of the arteries. Cerebral
Vascular Insufficiency or Transient Ischemia: Temporary Ischemia. Migraine Stroke: Account for a significant number
of strokes in young people, occur with migrane attacks, Appears as a transient ischemic attack. Symptoms: Impaired
sensory function, numbness of the skin, difficulties moving, aphasia. Cerebral Hemorrhage: Massive bleeding onto brain,
caused by hypertension/ high blood pressure. Angiomas and Aneurysms: Angiomas: COngenetal collection of abnormal
blood vessels that divert the normal flow of blood, Arteriovenous Malformation: masses of enlarged and tortuous cortical
vessels that are supplied by large arteries and drained by a large vein. Aneurysms: Vascular dilation: balloon expansion,
Congenital effects, hypertension, arteriosclerosis, embolisms or infections. Treatment of Vascular diseases: Prevention is
ideal. Drug therapies: Anticoagulants, Neuroprotectants to reduce cell death (calcium channel blockers), Antiplatelet agents
such as aspirin, Vasodilators, Steroids. Surgeries : Not usually practical, used to relive pressure after hemorrhage.
Traumatic brain injuries: Most common form of injury in people under the age of 40. Sport activities: 20%. In children and
elderly falls cause TBI, Higher incidence of head trauma in males between 15-30 years old. Affects brain functioning
through: Direct damage, Disrupting blood supply, Inducing bleeding, Swelling, Infection, Scarring of the brain. Traumatic
Brain Injuries: Open head injuries: TBIs with skull penetration, Neurological signs highly specific, May undergo rapid and
spontaneous recovery. Variety of Forces: Coup: Damage to the site of the blow, Contrecoup: damage at the opposite side of
the blow due to pushing or pressure. Twisting and shearing of the fibers, bleeding and pressure, edema. Closed head
injuries: Coma: Loss of consciousness commonly accompanies closed head injury. Behavioral effects: Impairment of
specific functions at the site of the damage. Generalized impairments from widespread trauma. General Complaints:
Inability to concentrate, bright people most affected, Effects on personality and social behavior. People who sustain closed
head injuries are at risk for future head injury. Cumulative effects. Behavioral Assessment in Head Injury: Glasgow
Coma Scale: of the degree of unconsciousness. Post Traumatic Amnesia: Measure of severity of injury, Correlates with
future memory disturbance, no consistent method for measurement. Recovery from Head Injury: Bulk of recovery occurs
in 6-9 months, Good recovery of cognitive skills but memory may never be as good as some other recovered functions. Poor
recovery of social functions and personality. Epilepsy: Recurrent seizures, Symptomatic Seizures: seizures identified with
a cause Idiopathic Seizures: Appear spontaneously. 3 common symptoms: Aura: warning of an impending seizure. Loss
of consciousness, movement. Four types of seizures. Focal Seizures: Begins in one place and spreads. Jacksonian focal
seizures: begins with movement in one part of the body and spreads. Complex partial seizures: Subjective experiences
before the attack, Automatisms(lip smacking, chewing), Postural changes. Generalized seizures: Bilaterally symmetrical
w/o focus. Tonic stage: body stiffens, breathing stops, Clonic Stage: rhythmic shaking. Postseizure or postictal stage:
confusion, may be preceded by an aura 50%. Akenetic seizuresz: seen in children, child may collapse without any warning.
Myoclonic spasms: Massive seizure, sudden flexion or extension of the body. Treatment of Epilepsy: Anticonvulsant
drugs: Diphenylhydantonin, Phenobarbital, Surgery. Tumors: Mass of tissue that persists and grows independently.
Benign: Not likely to return after seizure Malignant: Likely to recur after removal, Progressive and life threatening.
Encapsulated tumor: Distinct entity, puts pressure on the brain. Infiltrating tumor: Not separated from surrounding
tissue, May destroy cells or interfere with cellular functioning. Glioma: arise from glial cells, Meningioma Objective
indicator: Growths attached to the meninges Metastatic tumor: Occurs after a transfer of tumor cells from another part of
the body. TREATMENT: Surgery, Radiation. Headaches: Migraine: Classic migraine : aura that lasts for 20-40 min.
Occurs aas a result of vasoconstriction in the occipital cortex. Headache: Occurs as vasodilation takes place, Intense pain,
may be localized. May include nausea and vomiting. May last for hours or days. Common Migraine: Most frequent type,
occurs in 80% of migraine sufferers, No clear aura, but may get a signal of the attack. Cluster Headache: Unilateral pain.
Short duration but recurs. Headaches associated with Neurological diseases: Muscle contraction headaches:
Tension or nervous headaches, steady pain, may include anxiety, dizziness, or bright spots in front of the eyes.
Nonmigraines vascular headaches: Dilation of the cranial arteries, causes: fever, anoxia, anemia, high altitude, physical
effort, hypoglycemia, food or chemical agents. Treatments of Headaches: Migraine: Specific drugs at the time of the
attack, Ergotamine compounds- constrict arteries, given during acute attacks with caffeine. Tension headaches: Muscle
relaxant drugs, minor tranquilizers, posture improvement, reduction of stress. Infections: Invasion of the body by disease

producing microorganisms and the reaction of the tissue. How do infections kill neural cells? Interference with blood
supply, Disturb glucose or oxygen metabolism, alteration of cell membranes, formation of pus: increase pressure, change,
extracellular fluid, Edema. Viral Infections: Virus: Encapsulated aggregate of nucleic acis that is made of DNA or RNA.
Neurotropic Viruses: Virus with special affinity for CNS cells. Pantropic Viruses: Other body tissue and CNS tissue.
Bacterial Infections: Bacterium: Microorganism that has no chlorophyll and multiplies by simple division Meningitis:
Infection of the meninges by bacteria Brain abscesses: Secondary to infection elsewhere in the body, causes necrosis and
increases intracranial pressure. Mycotic infections: Invasion of the nervous system by a fungus. Parasitic Infections:
Amebiasis: Infestation of the protozoan ameba Entamoeba histolytica, Encephalitis and brain abscesses Malaria:
Transmitted by mosquito, produces local hemorrages and degeneration of neurons. Treatment of infections: Viral
Infections: Difficult to treat, no antidote. Except rabies Bacterial cerebral infections: Antibiotics, Drainage of abcesses or
spinal tap. Mycotic or parasitic infections: No satisfactory treatment, antibiotics. Myasthenia Gravis: Muscular fatigue,
more common in women, insufficient Ach receptors on the muscles. Treatment: Thymectomy and immunosuppressive
therapy. Multiple Sclerosis: Loss of myelin mainly in the motor tracts. Sclerotic plaques: Small, hard, circumscribed scars
where the myelin sheath has been destroyed. Proposed causes: Bacterial infection. Immune response. Environmental
factors. Vitamin D deficiency. Paraplegia: Paralysis of the lower limbs, Transection of the spinal cord. Immediate
symptoms: Loss of movement, sensation, and reflexes, Loss of thermoregulatory activity, Loss of bladder control, Spinal
reflexes gradually return. Hemiplegia: Loss of voluntary movement on one side of the body, changes in posture, and
changes in reflexes, Damage to neocortex and basal ganglia, Changes in reflexes, Appearance of the Babinski sign, Loss of
the abdominal reflex and in the cremasteric reflex in males PSYCHIATRIC DISORDERS PT1: Major Depressive
Disorder(MDD): One of the most common mental illnesses in the U.S., in 2012 16 million adults had at least 1 major
depressive episode. Mean age of onset is 32 years. Lifetime prevalence rate is 17%. MDD is more common in women. DSM
Criteria for MDD: Depressed mood or a loss of interest or pleasure in daily activities for more than two weeks. Mood
represents a change from the persons baseline. Impaired function: social occupational, educational. Specific symptoms at
least 5 of these 9, present nearly every day. Possible causes of MDD: sTrong genetic component , Highly heritable,
Concordance for monozygotic twins 70% whereas 20% for dizygotic twins. Researchers estimate heritability to be 40-50%.
Situations may lead to depression .Neurochemical aspects of depression: Reductions of monoamines: DA,NE, 5HT.
Brain derived neurotrophic factors: downregulated by stress, upregulated by antidepressants. May affect functioning of
monoamine synapses. Hypothalamic-Adrenal System: Oversecretion of cortisol; chronic stress, widespread influence on
cerebral functioning, kills cells in the hippocampus. Depression: Dexamethasone suppression test: can show excess
cortisol release, seen in suicide victims and depressed patients. Dexamethasone is a synthetic glucocorticoid, can suppress
cortisol release in normal people but not depressed patients. Neurochemical aspects of depression: Fluoxetine
(Prozac): SSRI, sustained cortisol kills hippocampal neurons, which could be due to lowered BDNF, Prozac stimulates BDNF in
the hippocampus. Gene x Environment: Role better to SSRI than CBT. Little evidence that SSRIs are effective in children
and adolescents. Bipolar disorder: Lifetime prevalence .4-1.6%, typical onset in 20s strong heratibility component.
Bipolar disorder is characterized by periods of depression alternating with expansive mood or mania. The rate of cycling
varies- rapid cycling consists of four or more cycles in one year. Some individuals may cycle several times in one day. Mood
Stabilizers: Lithium: Approved for US sale in 1970, normalizes mood in bipolar patients preventing both mania and
depressed mood swings(Increases serotonin and decreases norepinephrine), Can be safe or toxic, blood levels must be
monitored. (narrow safety margin, very low TI) Valproate: Increases GABA, used to treat epilepsy and migraines as well.
Anxiety Disorders: Characterized by excessive worry, fears or avoidance. EX. Panic disorders, specific phobias, social
phobias, PTSD, generalized anxiety disorder. Panic Disorders: Fear is the physiological reaction to immediate danger that
prepares us to fight or run away. When this physiological reaction is experienced in the absence of a threatening stimuli one
is having a panic attack, a panic attack is a discrete period in which there is a sudden onset of intense apprehension,
fearfulness or terror, often associated with feeling of impending doom. Strong arousal of sympathetic ANS: Heart
pounding, chest pain, sweating, shortness of breath, faintness, choking, fear of losing control or dying. Attack may occur: In
response to particular cue, without warning, In a situation where an attack previously occurred. Phobias: Specific phobia is
characterized by clinically significant anxiety provoked by exposure to a specific feared object or situation often leading to
avoidance behavior. Avoidance interferes with daily existence. The individual generally recognizes this fear is irrational.
Phobic disorders- Intense irrational fears centered on an object activity or situation that a person avoids. Agoraphobia:
fear of public places, Cynophobia: abnormal fear of dogs. Social Phobia: Characterized by clinically significant anxiety
provoked by exposure to certain types of social or performance situations often leading to avoidance behavior. PTSD: is
characterized by the re-experiencing of an extremely traumatic event accompanied by symptoms of increased arousal and
avoidance of stimuli associated with trauma. Probability of suicide and attempts increased as well as substance abuse
interpersonal problems, depression, guilt, and anger. Prevelance of PTSD by traumatic event: most of the people who do
develop PTSD have a family history of mental illness such as anxiety, depression or some other disorder. The fact that
concordance between monozygotic twins is higher than that of dizygotic twins lends further support to a genetic component.
True et al studied twin pairs who fought in Vietnam and found identical twins even shared more of the same symptoms than
fraternal twins. Generalized anxiety: Gad is characterized by at least 6 months of persistent and excessive anxiety and
worry. Anxiety isnt focused but its experienced much of the day sometimes for months or years. GAD affects about 5% of
the population age 15-45. Develops in teens/early adulthood and can persist for years. Individuals with GAD show signs of
constant worry and continuously predict anticipate, or imagine dreadful events. Life is generally stressful and minor events
provoke worry. Symptoms include: Muscle tension and agitation that leads to fatigue. Poor concentration, Irritability, sleep
difficulties, decreased pleasure. Treatment: Phobias: behavioral desensitization, one-session treatment. Social Phobia:
cognitive therapy that modifies negative of serotonin transporter (5-HTT) gene in depression?, Short allele means fewer
transmitters produced, leaving more 5-HT at synapse. Short/short allele leads to higher chance of getting depression. Gene
structure and function: Stressful or fearful information reaches the amygdala, which activates the subgenual ACC, which

activates dorsal ACC, which has inhibitory connection with amygdala. S/S or S/L 5-HTT individuals have decreased functional
connectivity of amygdala and subgenual ACC, as well as smaller volume of subgenual ACC. Circuit less effective in inhibiting
the amygdala. Blood flow and metabolic abnormalities in depression: Decreased activity in dorsolateral and medial
prefrontal regions(reduced memory and attention). Increased activity in Orbital regions, Amygdala (may increase HPA axis
activity through increasing cortisol). Treatment of MDD: Most antidepressant drugs suppress REM, but not all. Causal
relationship between REM and depression? Could be but incomplete story. Cognitive behavioral therapy: change
behaviors and thoughts: our thoughts influence our emotions, CBT equally as effective as antidepressant drugs. 80% relapse
rate for drug only treatment, CBT decreases this relapse rate. Most severe cases respond thoughts, plus social skills training.
Anxiolytics: Drugs that are used to relieve anxiety, relieve feelings of tension worry and signs of stress. Most anxiolytics are
CNS depressants, Benzodiazepines; Xanax, Ativan, Klonopin. Class I: Sedative-hypnotics and anti-anxiety agents: All
sedative hypnotics work by influencing the GABAa receptor. Alcohol and Barbituates: bind to the sedative hypnotic site and
increase the influx of Cl-, causing hyperpolarization. Higher dose=greater inhibitory effect. Benzodiazapines: bind to the
antianxiety site and enhance the binding of GABA to its receptors. PSYCHIATRIC DISORDERS PT 2 Overall efficacy of
treatment: Among psychological disorders, anxiety disorders are the most common and are associated with the
most impairment across various domains of functioning, including significant impairment of relationships, care giving and job
productivity. The current gold standard treatments for anxiety disorders are cognitive-behavioral therapy (CBT) and
pharmacotherapy. Though efficacious, 14-43% of anxiety disorder patients do not respond to treatment and 18-48%
relapse within 6 months. Schizophrenia: DSM-IV R Delusions or beliefs that distort reality. Hallucinations. Disorganized
speech, senseless rhyming. Disorganized, agitate behavior. Blunted emotions, loss of interest and drive. Monozygotic twins
are more likely to have anxiety through genetical exchange. Schizophrenia and development: an integrative model
suggests that schizophrenia will develop if a compromised brain is exposed to environmental stressors. Examples are
stresses of city life, prenatal exposure to influenza, and loss of oxygen at birth. Disorder chart: no disorder - spectrum
disorders -]schizotypy[-]schizophrenia. Schizotypal personality disorder signs and symptoms can include: being a
loner and lacking close friends outside of the immediate family. Incorrect interpretation of events, including feeling that
external events have personal meaning. Peculiar, eccentric or unusual thinking, beliefs or behavior. Dressing in peculiar ways.
Belief in special powers, such as telepathy. Perceptual alterations, in some cases bodily illusions, including phantom pains or
other distortions in the sense of touch. Persistent and excessive social anxiety. Peculiar style of speech, such as loose or
vague patterns of speaking or rambling oddly and endlessly during conversations. Suspicious or paranoid ideas,
hypersensitivity, and constant doubts about the loyalty and fidelity of others. Flat emotions, or limited or inappropriate
emotional responses. Types of schizophrenia: type 1 acute schizophrenia Positive symptoms (intrusive symptoms). This
type is more responsive to neuroleptics (anti-psychotics). Type 2 chronic schizophrenia Negative symptoms. Positive
symptoms - abnormal behaviors that are gained: hallucinations, delusions, excited motor behavior. Negative symptoms
are the result of lost functions: slow though and speech, emotional and social withdrawal, blunted affect or emotional
expression. Structural abnormalities in schizophrenic brains: less than average weight. Enlarged ventricles. Reduction
in the number of neurons the prefrontal cortex. Abnormal cellular structure in the prefrontal cortex and
hippocampus. Hypofrontality during card sorting. Biochemical abnormalities in schizophrenic brains: dopaminergic
function antipsychotics mainly act on the dopamine synapse. Glutamate. GABA. Brains of some schizophrenic patients
show structural changes. Cerebral ventricles become enlarged especially in males and remain so after the initial disease
onset. More enlarged ventricles predict a poorer response to drug treatment. The hippocampus and amygdala also differ in
schizophrenics they are way smaller. In schizophrenics pyramidal cells of the hippocampus have a disorganized arrangement.
This probably occurs during early cell development. Case studies: some studies show a loss of gray matter in the frontal
lobes, and PET scans shows less metabolic activity. The hypofrontality hypothesis - schizophrenia may be caused
by under activation of the frontal lobes. Typical neuroleptic drugs: all antagonists at dopamine D2 receptors. Dopamine
Hypothesis: Schizophrenia results from excess synaptic dopamine or increased postsynaptic sensitivity to it. Problems
with dopamine hypothesis: Schizophrenics have normal DA metabolite levels. Drugs block D2 receptors much faster than
symptoms are reduced. Some patients show no change. A new class of drugs that successfully treat schizophrenia does not
support the dopamine hypothesis. Atypical neuroleptics like clozapine: block serotonin receptors as well as D4 receptors.
Some actually increase dopamine levels in the frontal cortex. Motor disorders: Hyperkenetic: Increase motor activity.
Hypokenetic: Loss of movement. Hyperkenetic disorders: Huntingtons chorea: 1.6 per million worldwide, genetic
disorder (HTT gene). Intellectual deterioration and abnormal movements. Begins as a reduction of activity and a restriction of
interest. Involuntary movements begin about a year later. Autosomal dominant inheritance pattern: the mutated gene is
a dominant gene located on one of the nonsex chromosomes(autosomes). You only need one mutated gene to be affected by
this type of disorder. Movements: entail whole limbs, irregular, no pattern. Affect head, face trunk and limbs. Behavioral
symptoms: Personality changes, Cognitive impairments(recent memory, word fluency, slowed processing.) Anxiety,
depression, mania and schizophrenic-like psychoses. Brain abnormalities: Shrinkage of the cortex, atrophy of the basal
ganglia, imbalance among the various neurotransmitter systems. Death of GABA and Ach neurons in the basal ganglia. DA
cells no longer inhibited by GABA- become hyperactive- produce abnormal movements. Tourettes syndrome: 3 stages: 1.
Multiple tics 2. Inarticulate cries are added to the tics 3. Articulate words: Echolalia-repeating what others say, Coprolalia:
obscene or lewd speech. Age of onset 2-15. Not associated with neuroses, psychoses or other disorders. Presumed
subcortical origin- small cells in the basal ganglia. Treatment: Antidopemenergic drugs(haloperiodol), Norepinephrine
receptor agonists. Abnormalities in cognitive functions supported by the right hemisphere. Visuospatial (eg. Rey complex
figure task). Hypokenetic Disorders: Parkinsons disease(up to 1% worldwide) : degeneration of the substantia nigra,
loss of dopamine. Variety of symptoms that vary from patient to patient. Symptoms resemble changes in motor activity that
occur with age. 4 major symptoms: Rigidity, tremor, akinesia, postural disturbances. Positive symptoms: Resting
tremor, Muscular rigidity, Involuntary movements- Akathesia: cruel restlessness, Oculogyric crisis: Involuntary turns of the
head and eyes to the side. Negative symptoms: Disorders of posture: disorder of fixation: maintain part of body in

normal position. Disorder of equilibrium. Disorders of righting (standing, rolling), Disorders of locomotion:
Festination(once movement is initiated, faster and faster steps) Disorders of speech( absence of prosody),
Akenesia( lack of or slowness of movement). Progression of parkinsonism: Begins with tremors in the hand, Face
becomes masklike and movement slows. 10-20 years of progression prior to incapacitation. On again off again quality.
Causes: Idiopathic: Familial, part of the aging process. Viral origin. Drug induced: Ingestion of major tranquilizers. MPP+,
contaminant of synthetic heroin (MPTP). Psychological aspects of Parkinsons disease: Cognitive functions:
Generalized behavior slowing. Show symptoms similar to individuals with frontal lobe or basal ganglia lesions. Impaired on
the WAIS( digit span, block design) Treatment: Pharmacological therapy: Increase dopamine function(L-dopa). Block
cholinergic system(block involuntary movements).

Prefrontal Cortex (PFC)

higher cognition; communicate with

limbic system; planning; inhibition

fMRI and PET found decreased ac

in depressed; MRI found smaller
matter volume in depressed vs. c
(Drevets et al., 1997)

Hippocampus & Amygdala

learning, memory, emotion, communicate

with PFC; assign emotional significance to
stimuli

Increase in stress hormones causes c

death in HC (e.g., Kolb & Whishaw Fig
PET found increased activity of amyg
(Drevets et al., 1997)

(limbic system structures)