Discussion 8

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Physiology of Behavior

Twelfth Edition

Chapter 15

Neurological Disorders

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Tumors and Seizures

Cerebrovascular Accidents

Traumatic Brain Injury

Disorders of Development

Degenerative Disorders

Disorders caused by Infectious Disease

Tumors and Seizures

Cerebrovascular Accidents

Traumatic Brain Injury

Disorders of Development

Degenerative Disorders

Disorders caused by Infectious Disease

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Learning Objectives (1 of 5)

15.1 Describe the primary symptoms, causes, and treatments for brain tumors.

15.2 Describe the primary symptoms, causes, and treatments for seizures.

15.3 Explain how cerebrovascular accidents can occur.

15.4 Explain how treatments can be used to address the immediate and long-term symptoms of cerebrovascular accidents.

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Learning Objectives (2 of 5)

15.5 Identify some causes of traumatic brain injury.

15.6 Describe treatments for traumatic brain injuries.

15.7 Describe the effects of alcohol on development of the nervous system.

15.8 Contrast the symptoms, causes, and treatments of inherited metabolic disorders.

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Learning Objectives (3 of 5)

15.9 Identify symptoms, cause, and interventions for Down syndrome.

15.10 Describe how transmissible spongiform encephalopathies cause brain damage.

15.11 Describe the symptoms, causes, and treatments for Parkinson’s disease.

15.12 Describe the symptoms, causes, and treatments for Huntington’s disease.

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Learning Objectives (4 of 5)

15.13 Describe the symptoms, causes, and treatments for amyotrophic lateral sclerosis.

15.14 Describe the symptoms, causes, and treatments for multiple sclerosis.

15.15 Describe the symptoms, causes, and treatments for Alzheimer’s disease.

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Learning Objectives (5 of 5)

15.16 Describe the symptoms and causes of Korsakoff’s syndrome.

15.17 Identify the symptoms, causes, and treatments for encephalitis.

15.18 Identify the symptoms, causes, and treatments for meningitis.

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Tumors (1 of 4)

Tumor

Mass of cells whose growth is uncontrolled and that serves no useful function

Metastases

Process by which cells break off of a tumor, travel through vascular system, and grow elsewhere in body

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Tumors (2 of 4)

Malignant Tumor

Cancerous tumor

Lacks distinct border and may metastasize

Benign Tumor

Noncancerous tumor

Has distinct border and cannot metastasize

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Tumors (3 of 4)

Glioma

Cancerous brain tumor composed of one of several types of glial cells

Meningioma

Benign brain tumor composed of cells that constitute meninges

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Tumors (4 of 4)

Causes

Not from nerve cells

Tumor initiating cells

Treatments

Radiation

Chemotherapy

Surgery

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Figure 15.1 Benign and Malignant Tumors

Benign tumors are encapsulated. Malignant tumors lack encapsulation and infiltrate surrounding tissue. Cells from a malignant tumor can travel to new places in the body and cause additional tumors to grow.

Figure 15.1 page 484

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Figure 15.2 Compression in the Brain Due to a Benign Tumor

The photograph shows a slice of a human brain, showing how a large nonmalignant tumor (a meningioma) has displaced the right side of the brain toward the left. (The dashed line indicates the location of the midline.) The right lateral ventricle is almost completely occluded.

Figure 15.2, page 484

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Table 15.1 Examples of Types of Brain Tumors

Type of Tumor	Tumors arise from these cells:
Gliomas
Glioblastoma	Glial cells
Astrocytoma	Astrocytes
Ependymoma	Ependymal cells from the ventricles
Oligodendrocytoma	Oligodendrocytes
Meningioma	Cells of the meninges
Neurinoma	Schwann cells or cells of connective tissue covering cranial nerves
Angioma	Cells of blood vessels
Pinealoma	Cells of pineal gland

Table 15.1 page 485

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Figure 15.3 Types of Tumors (1 of 4)

(a) The photograph shows a slice of a human brain, showing a large glioma located in the basal ganglia, which has invaded both the left and right lateral ventricles.

Figure 15.3 page 485 (continued on next slide)

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Figure 15.3 Types of Tumors (2 of 4)

Figure 15.3 page 485 (continued on next slide)

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Figure 15.3 Types of Tumors (3 of 4)

(b) The photograph shows a midsagittal view of a human brain, showing a glioma located in the dorsal pons (arrowhead).

Figure 15.3 page 485 (continued on next slide)

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Figure 15.3 Types of Tumors (4 of 4)

(d) The CT scan of a brain shows the presence of a meningioma (round white spot indicated by the arrow).

Figure 15.3 page 485 (continued on next slide)

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Seizures (1 of 6)

Seizure Disorder

Preferred term for epilepsy

Convulsion

Violent sequence of uncontrollable muscular movements caused by seizure

Generalized Seizure

Seizure that involves most of brain

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Seizures (2 of 6)

Partial Seizure

Seizure that begins at focus and remains localized

Simple Partial Seizure

Partial seizure, starting from a focus and remaining localized

does not produce loss of consciousness

Complex Partial Seizure

Partial seizure, starting at a focus and remaining localized

produces loss of consciousness

See Table 15.2 in text page 486

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Seizures (3 of 6)

Aura

Sensation that precedes seizure whose exact nature depends on location of seizure focus

Absence

Type of seizure disorder often seen in children that is characterized by periods of inattention, which are not subsequently remembered

also called petit mal seizure

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Seizures (4 of 6)

Grand Mal Seizure

Generalized, tonic-clonic seizure, which results in convulsion

Tonic Phase

Seizure where patient’s skeletal muscles are contracted

Clonic Phase

Seizure where patient shows rhythmic jerking movements

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Seizures (5 of 6)

Status Epilepticus

Condition in which patient undergoes series of seizures without regaining consciousness

Damage appears to be caused by excessive release of glutamate during seizure (Thompson et al., 1996)

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Seizures (6 of 6)

Causes

Scarring from injury

Genetic factors

Drugs and infections

Treatments

Anticonvulsant drugs

Surgery

Scarring from injury: injury, stroke, dev abnormality, growing tumor

Genetic factors: some are idiopathic

Drugs and infections: that cause high fever

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Figure 15.4 Comparing Partial and Generalized Seizures

(a) Partial seizures affect localized regions. For example, the yellow region in (a) represents seizure activity limited to the primary motor cortex. This region of the brain was likely involved in Mrs. R.’s first seizure while waiting at the traffic light, when only her foot, leg, arm and then body began shaking. (b) Generalized seizures affect the whole brain. For example, the yellow region in (b) represents seizure activity throughout the brain.

Figure 15.4 page 487

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Figure 15.5 Primary Motor Cortex and Seizures

Mrs. R.’s seizure began in the foot region of the primary motor cortex, and as the seizure spread, more parts of her body became involved.

Figure 15.5, page 488

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Cerebrovascular Accidents: Causes (1 of 2)

Strokes

Hemorrhagic Strokes

Cerebrovascular accident caused by rupture of cerebral blood vessel

Ischemic Stroke

Cerebrovascular accident caused by occlusion of blood vessel

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Cerebrovascular Accidents: Causes (2 of 2)

Definitions and Concepts

Ischemia: Interruption of blood supply to region of body

Thrombus: Blood clot that forms within blood vessel, which may occlude it

Embolus: Piece of material that floats from one part of vascular system to block another part

Free Radical: Molecule with unpaired electrons; acts as powerful oxidizing agent; toxic to cells

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Figure 15.6 Strokes

(a) Formation of thrombi and emboli. (b) An intracerebral hemorrhage.

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Cerebrovascular Accidents: Treatments

Surgery

Anticoagulant drugs

Tissue plasminogen activator (tPA), Desmoteplase

Prevention: lifestyle factors and atherosclerotic plaques

Rehabilitation

tPA – only used in 3 hours, mixed results, issues of significant side effects and complications

Lifestyle risks: blood pressure, smoking, diabetes, cholesterol – Atherosclerotic plaques

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Traumatic Brain Injury: Causes (1 of 2)

Traumatic Brain Injury (TBI)

Serious health problem

US: 1.4 million annually treated in emergency department

Closed versus open head injuries

Traumatic brain injury can be caused by a projectile or a fall against a sharp object that fractures the skull, causing the brain to be wounded by the object or a piece of the broken skull.

Closed-head injuries do not involve penetration of the brain, but these injuries can also cause severe injury or death.

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Traumatic Brain Injury: Causes (2 of 2)

Chronic Traumatic Encephalopathy

Form of TBI

Neurodegeneration due to repeated head trauma

Media attention due to prevalence in athletes

Confirmed by postmortem examination

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Figure 15.11 Brain Changes in CTE

(a) This image shows a brain section from a patient with CTE (right) compared to a control section (left). The dark regions in the CTE section are areas where abnormal tau protein accumulated following brain injury. The white asterisk denotes dense accumulation of these proteins in the amygdala. (b) This image shows a diffusion tensor image scan of the corpus callosum from a control brain (in green, left) and the brain of a former professional boxer with CTE in (pink, right). The corpus callosum in the CTE patient’s brain shows damage (shorter and less extensive white matter tracts) associated with the brain injury.

(From Baugh, C. M., et al., Chronic traumatic encephalopathy: Neurodegeneration following repetitive concussive and

subconcussive brain trauma. Brain Imaging and Behavior, 2012, 6[2], 244–254.)

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Traumatic Brain Injury: Treatment

Reduce swelling and intracranial pressure

Assure adequate blood flow

Treat symptoms that develop after injury

Assess long term behavioral and cognitive changes

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Disorders of Development

Presence of toxic chemicals

Genetic abnormalities

Hereditary

Nonhereditary

Intellectual disability

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Disorders of Development: Toxic Chemicals

Teratogen

Fetal Alcohol Syndrome

Birth defect caused by ingestion of alcohol by pregnant woman

Neural Adhesion Protein

Protein that plays role in brain development

Teratogen: any chemical or toxin that results in abnormal development of an embryo

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Figure 15.12 Facial Malformation in Fetal Alcohol Syndrome

The photographs show a child with fetal alcohol syndrome, along with magnified views of mouse fetuses. (a) Mouse fetus whose mother received alcohol during pregnancy. (b) Typically-developing mouse fetus. (Photographs courtesy of Katherine K. Sulik.)

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Disorders of Development: Inherited Metabolic Disorders

Phenylketonuria (fee nul kee ta new ree uh)

Pyridoxine Dependency (peer i dox een)

Galactosemia (ga lak tow see mee uh)

Tay-Sachs Disease

Phenylketonuria (PKU) (fee nul kee ta new ree uh)

Hereditary disorder caused by absence of enzyme that converts amino acid phenylalanine to tyrosine: accumulation of phenylalanine causes brain damage unless special diet is implemented soon after birth

Pyridoxine Dependency (peer i dox een)

Metabolic disorder in which an infant requires larger-than-normal amounts of pyridoxine (vitamin B6) to avoid neurological symptoms

Galactosemia (ga lak tow see mee uh)

Inherited metabolic disorder in which galactose (milk sugar) cannot easily be metabolized

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Disorders of Development: Down Syndrome

Caused by presence of extra twenty-first chromosomes

Characterized by moderate-to-severe metal retardation

Often by physical abnormalities

chromosome; characterized by moderate to severe mental retardation and often by physical abnormalities

Congenital does not necessarily mean hereditary; it simply refers to disorder that one is born with

Down syndrome is caused not by inheritance of faulty gene but by possession of extra twenty-first chromosome

Down syndrome, described in 1866 by John Langdon Down, occurs in approximately 1 out of 700 births

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Figure 15.13 Karyotype of Down Syndrome

A karyotype allows a physician to examine the number of chromosomes present in a sample of genetic material. In this example, notice that there are three copies of chromosome 21. (red arrow) This is the karyotype of a female with Down syndrome.

Figure 15.13 page 498

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Table 15.3 Disorders of Development

Causes	Description	Symptoms
Exposure to Teratogens	Exposure to teratogens (such as alcohol) impairs brain development	Intellectual disability
Inherited Metabolic Disorders (PKU, pyridoxine dependency, galactosemia, Tay-Sachs disease)	Genetic abnormalities in the codes for specific enzymes. If untreated, leads to impaired brain development.	Intellectual disability; brain swelling in Tay-Sachs
Down syndrome	Three copies of the twenty first chromosome contribute to impaired brain development.	Intellectual disability; brain degeneration in adulthood.

Table 15.3 page 499

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Degenerative Disorders

Prion infection

Transmissible spongiform encephalopathies

Cognition

Alzheimer’s disease

Korsakoff’s syndrome

Motor Behavior

Parkinson’s disease

Huntington’s disease

Amyotrophic lateral sclerosis

Multiple sclerosis

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Transmissible Spongiform Encephalopathies

Transmissible Spongiform Encephalopathy (TSE)

Prion (pree on)

Sporadic Disease

Caspase

“Killer enzyme” that plays role in apoptosis, or programmed cell death

Accumulation of misfolded, abnormal proteins signals for apoptosis and production of caspases

Transmissible Spongiform Encephalopathy

Contagious brain disease whose degenerative process gives brain spongelike appearance; caused by accumulation of misfolded prion protein

Prion (pree on)

Protein that can exist in two forms that differ only in their three-dimensional shape: accumulation of misfolded prion protein is responsible for transmissible spongiform encephalopathies

Sporadic Disease

Disease that occurs rarely and is not obviously caused by heredity or infectious agent

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Figure 15.14 Misfolded Proteins

Figure 15.14 page 500

The sequence of amino acids of normal prion protein (PrPc) and infectious prion (PrPSc) are identical.

Why different effects?

The answer is that the functions of proteins determined by three-dimensional shapes. (way the protein is folded)

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Parkinson’s Disease

Tremors

Vibratory movements of arms and hands that diminish somewhat when individual makes purposeful movements

Accompanied by joint rigidity

Not displayed in all patients

Important degenerative neurological disorder, Parkinson’s disease is caused by degeneration of the nigrostriatal system—the dopamine-secreting neurons of the substantia nigra that send axons to the basal ganglia.

The primary symptoms of Parkinson’s disease are muscular rigidity, slowness of movement, a resting tremor, and postural instability.

Parkinson’s disease is seen in approximately 1 percent of people over 65 years of age.

Parkinson’s disease also produces a resting tremor—vibratory movements of the arms and hands that diminish somewhat when the individual makes purposeful movements.

The tremor is accompanied by rigidity; the joints appear stiff.

However, the tremor and rigidity are not the cause of the slow movements.

In fact, some patients with Parkinson’s disease show extreme slowness of movements but little or no tremor.

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Parkinson’s Disease: Causes (1 of 2)

Lewy Body

alpha-Synuclein

Toxic Gain of Function

Genetic disorder caused by dominant mutation that involves faulty gene that produces protein with toxic effects

Loss of Function

Genetic disorder caused by recessive gene that fails to produce protein that is necessary for good health

Lewy Body

Abnormal circular structures with dense core consisting of -synuclein protein; found in cytoplasm of nigrostriatal neurons in people with Parkinson’s disease

-Synuclein

Protein normally found in presynaptic membrane, where it is apparently involved in synaptic plasticity: abnormal accumulations are apparently the cause of neural degeneration in Parkinson’s disease

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Parkinson’s Disease: Causes (2 of 2)

Parkin

Protein that plays role in ferrying defective or misfolded proteins to proteasomes

Mutated parkin is cause of familial Parkinson’s disease

Proteasome

Organelle responsible for destroying defective or degraded proteins within the cell

Ubiquitin

Protein that attaches itself to faulty or misfolded proteins and thus targets them for destruction by proteasomes

Figure 15.16 page 502

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Figure 15.15 Lewy Bodies

A photomicrograph of the substantia nigra of a patient with Parkinson’s disease shows a Lewy body, indicated by the arrow.

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Figure 15.16 The Role of Parkin in Parkinson’s Disease

Parkin is involved in the destruction of abnormal or misfolded proteins by the ubiquitin-proteasome system. If parkin is defective because of a mutation, abnormal or misfolded proteins cannot be destroyed, so they accumulate in the cell. If α-synuclein is defective because of a mutation, parkin is unable to tag it with ubiquitin, and it accumulates in the cell.

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Parkinson’s Disease: Treatment (1 of 2)

Drug Treatments

L-DOPA

Precursor for dopamine

Deprenyl

Stereotaxic procedures

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Parkinson’s Disease: Treatment (2 of 2)

Surgical procedures and deep brain stimulation

Internal Division of the Globus Pallidus (Gpi)

Division of globus pallidus that provides inhibitory input to motor cortex via thalamus

Sometimes stereotaxically lesioned to treat symptoms of Parkinson’s disease

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Figure 15.17 Pharmacological Treatment Strategies for Parkinson’s Disease

Figure 15.17 page 504

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Figure 15.18 Connections of the Basal Ganglia

This schematic shows the major connections of the basal ganglia and associated structures. Excitatory connections are shown as black lines; inhibitory connections are shown as red lines. Many connections, such as the inputs to the substantia nigra, are omitted for clarity. Two regions that have been targets of stereotaxic surgery for Parkinson’s disease—the internal division of the globus pallidus and the subthalamic nucleus—are outlined in blue. Damage to these regions reduces inhibitory input to the thalamus and facilitates movement. Deep brain stimulation of these regions produces similar effects.

Figure 15.18 page 505

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Figure 15.19 Deep Brain Stimulation

Electrodes are implanted in the patient’s brain, and wires are run under the skin to stimulation devices implanted near the collarbone.

(Based on Okun, M. S., Deep-brain stimulation for Parkinson’s disease, New England Journal of Medicine, 2012,

367[16], 1529–1538.)

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Huntington’s Disease (1 of 2)

Basal ganglia disease

Caused by degeneration of the caudate nucleus and putamen

Characterized by progressively more severe uncontrollable jerking movements, writhing movements, dementia, and finally death

At present, there is no treatment for Huntington’s disease

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Huntington’s Disease (2 of 2)

Huntington’s Disease Symptoms

Begin in person’s thirties and forties, sometimes in early twenties

Movements look like fragments of purposeful movements, occur involuntarily

Disease is progressive

Death usually occurs within ten to fifteen years after symptoms begin

Symptoms of Huntington’s disease usually begin in person’s thirties and forties, but can sometimes begin in early twenties

Movements of Huntington’s disease look like fragments of purposeful movements but occur involuntarily

Disease is progressive, includes cognitive and emotional changes, and eventually causes death, usually within ten to fifteen years after symptoms begin

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Figure 15.20 Brain Tissue Loss in Huntington’s Disease

Comparison of a normal brain (left) with that from a patient who died with Huntington’s disease

Figure 15.20 page 506

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Huntington’s Disease: Causes

Hereditary disorder, caused by dominant gene on chromosome 4

Defect identified as repeated sequence of bases that code for amino acid glutamine (Collaborative Research Group, 1993)

Abnormal huntingtin is cause of Huntington’s disease

Huntington’s disease is hereditary disorder, caused by dominant gene on chromosome 4

Gene has been located, and its defect has been identified as repeated sequence of bases that code for amino acid glutamine (Collaborative Research Group, 1993)

Huntingtin (HTT) is protein that may serve to facilitate production and transport of brain-derived neurotrophic factor: abnormal huntingtin is cause of Huntington’s disease

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Figure 15.22 Infection with Abnormal Huntingtin

The photomicrograph shows two neurons that have been infected with genes that express fragments of abnormal huntingtin. The lower neuron shows an inclusion body (orange), and the upper one does not. Arrasate et al. (2004) found that neurons with inclusion bodies survived longer than those without inclusion bodies. Blue ovals are thenuclei of uninfected neurons.

Figure 15.22, page 508

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Amyotrophic Lateral Sclerosis

Degenerative disorder that attacks spinal cord and cranial nerve motor neurons

Incidence

Symptoms and course of disorder

Causes: Hereditary versus sporadic

Treatment

Amyotrophic lateral sclerosis (ALS) is degenerative disorder that attacks spinal cord and cranial nerve motor neurons (Zinmon and Cudkowicz, 2011)

Incidence of this disease is approximately 5 in 100,000

Symptoms include spasticity (increased tension of muscles, causing stiff and awkward movements), exaggerated stretch reflexes, progressive weakness and muscular atrophy, and, finally, paralysis

Death usually occurs between five and ten years after onset of disease as result of failure of respiratory muscles

Muscles that control eye movements are spared and cognitive abilities are rarely affected

Ten percent of cases of ALS are hereditary; the other ninety percent are sporadic

Of the hereditary cases, 10–20 percent are caused by mutation in gene that produces enzyme superoxide dismutase 1 (SOD1), found on chromosome 21

Treatment

The only current pharmacological treatment for ALS is riluzole, a drug that reduces glutamate-induced excitotoxicity, probably by decreasing the release of glutamate

Patients live two months longer

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Multiple Sclerosis

Autoimmune demyelinating disease

Transmission of neural messages

Variety of neurological disorders

Symptoms and progression

The immune system attacks the myelin sheath.

This occurs at scattered locations within central nervous system.

Process leaves hard patches of debris called sclerotic plaques.

Normal transmission of neural messages through demyelinated axons is interrupted

Because damage occurs in white matter located throughout the brain and spinal cord, a wide variety of neurological disorders are seen

Symptoms of multiple sclerosis often flare up and then decrease, to be followed by another increase in symptoms after varying periods of time

In most cases, this pattern (remitting-relapsing MS) is followed by progressive MS later in course of the disease

Progressive MS is characterized by slow, continuous increase in symptoms of disease

Figure 15.23, page 509

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Figure 15.23 Multiple Sclerosis

In this slice of the brain of a person who had multiple sclerosis, the arrowheads point to sclerotic plaques in the white matter.

(Courtesy of A. D’Agostino, Good Samaritan Hospital, Portland, Oregon.)

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Multiple Sclerosis: Treatment

Only two treatments for multiple sclerosis have shown promise (Aktas, Keiseier, and Hartung, 2009)

Interferon beta

Glatiramer acetate (also known as copaxone or copolymer-1)

Interferon , a protein that modulates responsiveness of immune system

Another partially effective treatment is glatiramer acetate (also known as copaxone or copolymer-1)

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Dementia (1 of 4)

Caused by several disorders

Lewy bodies

Alzheimer’s disease

Occurs in 10% of the population over 65, almost 50% over age 85 – most common cause of dementia

Degenerative brain disorder of unknown origin; causes progressive memory loss, motor deficits, and eventual death

Characterized by progressive loss of memory and other mental functions

They eventually become bedridden, then become completely helpless, and finally succumb (Terry and Davies, 1980)

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Dementia (2 of 4)

Alzheimer’s disease

Degenerative brain disorder of unknown origin

Causes progressive memory loss, motor deficits, and eventual death

Amyloid Plaque (amm i loyd)

-Amyloid (A)

Neurofibrillary Tangle (new row fib ri lair y)

-Amyloid Precursor Protein (APP)

Secretase (see cre tayss)

Amyloid Plaque (amm i loyd)

Extracellular deposit containing dense core of -amyloid protein surrounded by degenerating axons and dendrites and activated microglia and reactive astrocytes

-Amyloid (A)

Protein found in excessive amounts in brains of patients with Alzheimer’s disease

Neurofibrillary Tangle (new row fib ri lair y)

Dying neuron containing intracellular accumulations of abnormally phosphorylated tau-protein filaments that formerly served as cell’s internal skeleton

-Amyloid Precursor Protein (APP)

Protein produced and secreted by cells that serves as precursor for -amyloid protein

Secretase (see cre tayss)

Class of enzymes that cut -amyloid precursor protein into smaller fragments, including -amyloid

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Dementia (3 of 4)

Alzheimer’s Disease: Causes

Some forms hereditary

Presenilin (pree sen ill in) gene

Apolipoprotein E (ApoE) (ay po lye po proh teen) gene mutation

Level of education and lifestyle

Amyloid Plaque

Extracellular deposit containing dense core of -amyloid protein surrounded by degenerating axons and dendrites and activated microglia and reactive astrocytes

Presenilin (pree sen ill in)

Protein produced by faulty gene that causes -amyloid precursor protein to be converted to abnormal short form; may be a cause of Alzheimer’s disease

Apolipoprotein E (ApoE) (ay po lye po proh teen)

Glycoprotein that transports cholesterol in blood and plays role in cellular repair: presence of the E4 allele of apoE gene increases the risk of late-onset Alzheimer’s disease

Education

A report by Bennett et al. (2003) found a positive relationship between increased number of years of formal education and cognitive performance, even in people whose brains contained significant concentrations of amyloid plaques

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Dementia (4 of 4)

Alzheimer’s Disease: Treatment

Acetylcholinesterase inhibitors

NMDA receptor antagonist

Immunological research is promising

Only approved are:

Acetylcholinesterase inhibitors (donepezil, rivastigmine, and galantamine)

NMDA receptor antagonist (memantine)

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Figure 15.24 Alzheimer’s Disease

(a) Dorsal view of the brain of a person with Alzheimer’s disease.

Note that the sulci are especially wide, indicating degeneration of the cortex. (b) Dorsal view of a normal brain.

Figure 15.24, page 510

Alzheimer’s disease produces severe degeneration of the hippocampus, entorhinal cortex, neocortex (especially the association cortex of the frontal and temporal lobes), nucleus basalis, locus coeruleus, and raphe nuclei.

Figure 15.24 shows photographs of the brain of a patient with Alzheimer’s disease and of a normal brain.

You can see how much wider the sulci are in the patient’s brain, especially in the frontal and temporal lobes, indicating substantial loss of cortical tissue

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Figure 15.25 Microscopic Features of Alzheimer’s Disease

The photomicrographs from deceased patients with Alzheimer’s disease show (a) an amyloid plaque, filled with β-amyloid protein, and (b) neurofibrillary tangles.

(Photos courtesy of D. J. Selkoe, Brigham and Women’s Hospital, Boston.)

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Figure 15.26 β-Amyloid Protein

The schematic shows the production of β-amyloid protein (Aβ) from the amyloid precursor protein.

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Figure 15.28 Immunization Against Aβ

The graph shows the effect of immunization against Aβ on the cognitive decline of patients who generated Aβ antibodies (successfully immunized patients) and those who did not (controls).

(Based on data from Hock et al., 2003.)

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Korsakoff’s Syndrome

Neither hereditary nor contagious

Caused by environmental factors—usually (but not always) involving chronic alcoholism

Disorder actually results from thiamine deficiency

Causes anterograde amnesia

Damage occurs in mammillary bodies, located at base of brain, in posterior hypothalamus

Thiamine is essential for step in metabolism: carboxylation of pyruvate, intermediate product in breakdown of carbohydrates, fats, and amino acids

Although degeneration is seen in many parts of brain, the damage characterizes this disorder occurs in mammillary bodies, located at base of brain, in posterior hypothalamus. (See Figure 15.28)

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Figure 15.29 Korsakoff’s Syndrome

This brain slice shows the degeneration of the mammillary bodies in a patient with Korsakoff’s syndrome.

(Courtesy of A. D’Agostino, Good Samaritan Hospital, Portland, Oregon.)

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Disorders Caused by Infectious Diseases: Encephalitis (1 of 2)

Inflammation of brain caused by bacteria, viruses, or toxic chemicals

Herpes Simplex Virus

Virus that normally causes cold sore near lips, but can also cause brain damage

Encephalitis can also be caused by HSV

Viral encephalitis also caused by polio (acute anterior poliomyelitis) and rabies (see next next slide)

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Disorders Caused by Infectious Diseases: Encephalitis (2 of 2)

Rabies

Fatal viral disease that causes brain damage and is usually transmitted through bite of infected animal

Acute Anterior Poliomyelitis

Viral disease that destroys motor neurons of brain and spinal cord

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Figure 15.30 Meningitis and Encephalitis

Figure 15.30 page 516

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Disorders Caused by Infectious Diseases: Meningitis

Inflammation of meninges

can be caused by viruses or bacteria

Another category of infectious diseases of brain actually involves inflammation of meninges, layers of connective tissue that surround central nervous system

Discussion 8

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