W11. Chapter21. Nervous System Flashcards

1
Q

Nervous System consists of

A
  • Brain and spinal cord
  • peripheral nervous system (peripheral nerves, autonomic ganglia)
  • closely interrelated with the endocrine system and skeletal muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Brain includes

A

-cerebrum, cerebellum, brain stem. Can be further seperated to the midbrain, pons, and medulla oblongata

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Largest part of the brain

A
  • the cerebrum.
  • Is separated into 2 hemespheres, which are connected through a number of commissures, most prominent is corpus callosum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the giri and sulci

A
  • external surface of the brain is arranged into giri, which are separated by invaginations called sulci
  • giri is composed predominently by grey matter -cortex
  • brain tissue beneat the cortex is called white matter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Deep part of the brain

A
  • also contain grey areas- form basal ganglia, thalamus, and hypothalamus
  • cortex and subcortical gray matter are composed of numerous neurons and support cells
  • the axons extend into the white matter where they are mylenated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Lobes of the cerebrum

A
  • frontal: motor functions, behavior, emotions, intelect
    parietal: sensory
    temporal: hearing and smelling
    occipital: visual
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What do the basal ganglia do?

A

-supply inhibitory stimuli to skeletal muscles, coordinate skeletal muscle contraction, block unwanted muscle contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Function of the thalamus

A
  • nb for integrating sensory stimuli
  • nb determinant for conciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Function of the hypothalamus

A
  • crossroad that connects different parts of the brain
  • involved in body functions: bp, temp reg, hr, thirst
  • source of neurosecretory substances that stimulate the pituitary to produce tropic hormones- regulating the function of endocrine glands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Midbrain, pons, and medullaoblongata

A
  • contain numerous mylenated nerve bundles
  • regulate elementary body functions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Function of the cerebellum

A
  • major regulator of motor activities
  • receives sensory input from the spinal cord and vestibular organ of the inner ear, as well as motor impulses brom the cerebral cortex
  • damage affects coordination of limb and eye movements
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Components of the spinal cord

A
  • consists fo grey and white matter. Grey matter located internal to the white matter, around the central canal
  • grey matter has butterfly like shape on cross section, with posterior and anterior horns that consist of neurons and unmyelenated nerve fibers

tracts- p.469

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Peripheral and Autonomous nervous system

A

p.469

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

The brain is enveloped by

A

-menenges- specialized connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Facts of the Nervous system:

Consists of highly specialized functional units

A
  • loss of certain parts of CNS results in certain loss of function defects
  • irreversible, since neurons dont regenerate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Facts of the nervous system:

CNS is protected by bones of scull and vertebrae

A
  • skull encloses the brain and sheilds it
  • brain wounds occur if integrety of the skull is disrupted
  • vertebrae are linked together by intervertibral disks and tendons that allow for a certain degree of mobility
  • spinal cord therefore more suseptible to external trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

facts of the nervous system: Seperation of CNS from remainder of body

A
  • by menenges and blood brain barrier
  • CNS has an abundant blood supply - which ensures constant supply of energy.
  • brain must remain relatively isolated from the metabolic functions of the body that may adversely affect neurons
  • blood brain barrier acts like a filter, allowing some pasage of substances from blood to CSF ex. bilirubin does not enter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Functions of CSF: Brain

A
  • separate brain from meneges
  • mechanical buffer between brain and bones of skull
  • serves as venue for disposition of waste products and metabolites from the brain. Normally, its composition does not fluctuate much. Ex. neutrophils in menengitis
  • Production, flow, and resorption of CSF remains constant. Obstruction can lead to hydocephalus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Principal Cells of the CNS

A
  • Neurons: non-invading, post-mitotic, permanent cells
  • Glial cells: support the neurons, faculative and mitotic, capable of dividing when stimulated
  • contains billions of neurons, all of which are formed in prenatal intrauterine life. neurons are long lived cells. Loss of neurons can not be replaced b/c remaining neurons can not divide, and brain does not have reserve. therefore, every lost of brain substance results in permanent defect.
  • glial cells: retain capacity for multiplication, and can multiply in response to certain forms of injury. Ex. Gliosis, increased number of glial cells, in repsonse to brain injury. Found around brain tumors, foci of intracerebral hemmorhages, brain infarct.
  • b/c adult neurons are incapable of dividing, adult brain cancers orginate from glial cells (glioma). In children, malignant cells of neural cell origin originate from undifferentiated precursors of neural cells.
  • menenges and blood vessels of the brain can proliferate and cause tumors (menengioma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Facts about the CNS and Diseases

A
  • The CNS can be affected by diseases that involve other organs, or by diseases that are unique to the CNS
  • especially circulatory, metabolic and infectious
  • diseases restricted to the brain may be caused by neurotropic pathogens or b/c of metabolic changes unique to neural cells. Ex. rabies is neurotropic virus which infects only nerve cells. Ex. neurodegeneration in Parkinsons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Increased intracranial pressure from cerebral edema may lead to

A

may lead to loss of conciousness, progressing to coma or death

  • brain edema may be caused by multiple brain lesions, intracranial hemmorhage, inflammation, and numerous metabolic or circulatory disturbances such as shock
  • increased ICP is a life threatening condition
  • symptoms depend on the pace
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

A rapid, but gradual increase in ICP withh result in

A
  • severe headache that ususally accompanied by vomiting, blurry vision, and loss of conciousness
  • these patients usually lapse into a coma, and die of apnea as a result of inhibition of medulary vital centers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Death from increased ICP result from

A
  • compression of vital centers in the brainstem
  • most often, the centers of the medula oblongata are compressed by the edematous tonsils of the cerebellum, which herniates through the foramen magnum
  • herniation of the medial portion of the cerebral hemisphere beneath the tentorium cerebilli may compress pons and also cause death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Symptoms of CNS dysfunction

A

-some may result from subtle changes in brain cells that can not be recognised microscopically. Ex schizophrenia - no seen pathological changes-occur at subcellular level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Developmen of CNS (normally)

A
  • CNS develops from the neural plate, which folds and closes into a neural tube extending along the dorsal side of the body axis.
  • As the neural tube forms, it becomes internalized and is protected by the overlying skin
  • the mesenchyme between the skin and the neural tube is induced to form bone- which gives rise to the skull and vertebrae, which finally encase the spinal cord
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What gives rise to dysraphic disorders

A
  • incomplete fusion of the neural tube, and defective formation of the menenges, calvaria, or vertebrae
  • If the calvaria are not formed, and the brain is destroyed in-utero, the malformation is anencephaly.

Milder dysraphic malformations, such as meningocele, myelome-ningocele, and spina bifida, are characterized by a lack of fusion of the posterior bone coverings.

If the meninges protrude through the bony defect, the malformation is called meningocele. I

n myelomeningocele, the protrusion contains not only the meninges, but also a portion of the spinal cord.

Spina bifida is characterized by an absence of vertebral arches, resulting in exposure of the meninges or the spinal cord to the outer world.

Spina bifida may be evident at birth as a deep defect on the lower back, or it may be covered with skin and be inapparent (spina bifida occulta)”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Intracrainial Hemmorhages: Classifications

A
  • epidural
  • subdural
  • subarachnoid
  • intracerebral
  • may be caused by trauma, contusions, rupture of blood vessels (anuerism or HTN), or abnormalities of coagulation (congential or aquired bleeding disorders).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Dysraphic Developmental Disorders: Image

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Hematoma: Image

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Epidural Hematoma

A
  • located in the space between the scull and the dura, in a space that in under normal circumstances doesnt exist, b/c of close proximity between dura and the skull bones
  • develop from ruptured meningeal artery, most often torn by a bone spindle resulting from a fracture of temporal bone
  • arterial blood slowly fills the space, and separates the dura from the bone. Takes several hours before large hematomas are formed
  • Once 50-60ml, it is large enough to compress the brain and cause coma
  • in children, whose bones are not firmly fixated, arterial rupture can occur b/c of traumatic bone displacement
  • can be lethal if not recongnized
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Subdural Hematomas

A
  • space between the dura and arachnoid
  • normally this space is bridged by thin-walled veins, that can be torn easily by trauma- especially blunt trauma which causes sudden movement of brain in one direction, and the dura in another
  • found in boxers, and unattended bed ridden patients
  • symptoms are non-specific, headache, but as it enlarges - may cause coma or death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Subarachnoid Hemmorhages

A
  • located in the space between the arachnoid and the pia (ie-brain surface)
  • most often caused by traumatic contusion of the brain, blood leaks into the subarachnoid space from ruptured cerebral blood vessels at the base of the brain
  • ruptured aneurisms of the Circle of Willis are another important cause. These congenital berry aneurisms are found in 1-2% of the population, most are silent. Rupture between 30-60yo, can be precipitated by HTN, but most often no obvious cause.
  • bleeding into subarachnoid space associated with high mortality
  • if recognised, berry aneurisms can be tx. surgically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Intracerebral Hemmorhage

A
  • common complication of head trauma
  • contusion of brain and rupture of intracerebral blood vessels
  • non-traumatic causes include stroke, leukemia and other clotting disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Cerebrovascular Disease

A
  • 3rd most common cause of death and most crippling disease in the USA
  • Most common clinical manifestation is stroke
  • Stoke: ischemic (85%-r/t atherosclerosis or thromboembolic occlusion of the cerebral arteries), (15% hemmorhagic, complicaton of htn).
  • Atherosclerosis: narrowing may be gradual or may be sudden, may be widespread or localized lesions.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Cerebrovascular Disease: Global Ischemia

A
  • widespread atherosclerotic narrowing of entire cerebrovascular system develop multiple foci of ischemic necrosis
  • such lacunar infarcts cause minor neurologic deficits, but over time will cause mental deterioration
  • cardiac failure or other forms of vascular collapse, results in widespread infarcts
  • these hypoperfusion infarcts located in parasagital cortex
  • hypoperfusion leads to laminar necrosis of the deeper zones of the grey matter. -Blood does not get to the deep areas
  • If blood flow restores, patients can recover with only minor deficits.

But even minor CVAs can have a cumulative effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Most common cause of cerebral infarct

A
  • thrombocclusion of an atherosclerotic artery
  • thromboemboli of heart chambers or valves the second most common cause

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Cerebral Infarct: Pathologic changes in the brain

A
  • depends on time that has elapsed between onset of occlusion
  • ischemic brain liquifies and ichemic part undergoes necrosis
  • encephomalacia is the softening of the brain, may remain pale or may be red from collateral circulation and transform into a hemmorhagic infarct
  • red infarcts are more common after cerebral embolization with arterial thromboemboli because these infarcts are more readily perfused from asdjasent non-infarcted vessels
  • brain tissue is edematous. During phase of maximal cerebral swelling, the patients are at risk of dying
  • within a few days, swelling goes down, and patients have a better chance of surviving. Margins of the viable tissue become vascularized
  • necrotic tissue is removed by scavenger cells
  • infarct turns into a fluid filled cavity (pseudocyst)
  • brain infarcts cannot heal, and the neurological deficits caused by them are permanent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Clinical Presentation of Cerebral Infarct

A
  • Depends on location
  • Occlusion of middle cerebral artery is most common cause, contralateral hemiplegia, sensory loss on the same side of the body, bilateral symmetric loss of vision in half of the visual fields, with eyes deviating to the side of the lesion.
  • Global aphasia occurs if the infarct occurs in the dominant hemisphere
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Treatment of Stroke

A
  • life supportive measures
  • brain edema: corticosteroids, dehydrating hyperosmolar agents that drain fluid from brain into circulation
  • physical therapy as part of long term rehab, OT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Location of Infarcts: Image

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Prognosis with stroke: %

A
  • 80% of people survive initial stroke
  • 60% are alive 3 years after
  • 25% chance of having another stroke
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Intracerebral Hemmorhage

A
  • in patients with no vascular abnormalities, most often caused by arterial htn
  • ruptured small vessels that have been damaged mechanically by HTN
  • most common sites are basal ganglia (2/3)
  • Cerebellar or pontine account for rest
  • Intracerebral hemmorhage results in a well circumscribed hematoma that is visible on CT. They are surrounded by edematours brain tissue. Infarct turns into a pseudocyst, containing hemosiderin-laden macrophages.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Clinical Features of Intracerebral Hemmorhage

A
  • may resemble cerebra infarction, but clinical picture is more dramatic. 30% of patients losing conciousness and appearing stricken
  • Severe headache and urge to vomit
  • Hemmorhage into basal ganglia= rapid onset of hemiplegia and hemiparesis,
  • Cerebellar hemmorhage= presents with loss of balance, nausea, vomiting, and severe headache. Patients lapse into coma and usually die within 48 hrs.
  • Pontine hemmorhages= lethal, most die within hours
44
Q

Treatment of hypertensive intracerebral hemmorhage

A
  • supportive
  • depends on site
45
Q

Classificantions of brain injury

A
  • contusion, concussion, laceration
  • often accompanied by hematomas
46
Q

Head injury:image

A
47
Q

Brain: Concussion

A
  • presents as a transient loss of conciousness, usually after blunt trauma
  • loss of conciouness is based on functional disturbances affecting the temporal lobe and reticular activating system of the brainstem
  • no significant macroscopic or microscopic changes to brain or brainstem
48
Q

Brain Contusion

A
  • bruise
  • characterized by disruption of cerebral or meningeal blood vessels by severe blunt trauma
  • lesions are hemmorhagic and typically located at the site of impact (coup lesion), and its diametrically opposite pole (countercoup)
  • contracoup is the result of decelleration of the moving brain caused by the skull bones that serve as shock absorbers
  • rotation of the head on impact causes more damage
  • brain contusions are serious injuries with considerable mortality
  • survicors will have neuro deficits, some being permanent
49
Q

Brain Laceration

A
  • typically caused by open trauma that disrupts the intergrity of the brain
  • gunshot wounds that lacerate the brain tissue.
  • Death is r/t expansion of intracranial volume and consequent compression of vital centers in the brainstem
  • pts who survive have major neur deficits, and epilepsy
50
Q

Injuries of the cervicle spine: classified as

A

hyperextension injury: impact on forehead causes hyperextension and rupture of the anterior spinal ligaments, with subsequent compression of the posterior side of the spinal cord

Hyperflexion injury: impact on the occiput causes extensive anterior flexion of the spinal cord and compression of the anterior portion of the spinal cord

both may cause complete transection of the spinal cord, resulting in loss of motor and sensory functions below the injury. Typically flacid paralysis accompanied by loss of sensation. Urination and defecation reflexes are lost

-with time, reflexes functions return and the paraplegia or quad becomes spastic. Reflexes with bladder and bowel may partically restored

51
Q

Primary causes of infection in CNS

A
  • bacterial:
  • viral: herpes most common in usa, west nile 10-20%, rabies
  • protazoal
  • fungal
52
Q

Bacterial Infections of the Brain

A
  • typically develop hematologically, during sepsis, bacteremia, and septic emboli
  • open wounds of the brain are usually by bacteria that have gained direct entrance to brain parenchyma
  • bacterial infections of the paranasal sinuses or middle ear can also spread to cranium and cause cns infection
  • streptococcus pneumoniae accounts for most bacterial menigitis in adults
  • Group B strep, in female urogenital tract can infect babies during childbirth and result in bacterial menigitis of neonates. Can also be caused by Ecoli and listeria.
  • most nb bacterial pathogen in children, adolescents, and older adults are Neisseria M. (Meningecoccus) and S. Pneumoniae. Result in mini-epidemics in close cluters (ex. baracks).
53
Q

Bacterial Infections: Image

A
54
Q

Pathology of encephalitis

A
  • may present as local or diffuse
  • most often cause by viruses that invade neural or glial cells
  • ex. herpes infects the temporal lobe causing foci of necrosis and hemmorhage (local)
  • ex. west nile -accompanied by widespread lymphocytic infiltrates that fill perivascular Virchow-Robin spaces and can be readily recognised by microscopic exam of brain on autopsy
  • ex. Myelitis is diffuse infection of the spinal cord ex. Poliomyelitis
55
Q

Cerebral Abscess of the brain

A
  • localized suppurulative infection of the brain
  • mass lesion, may be mistaked for tumor
  • cavity filled with puss and capsule filled with glial cells and firboblasts
  • most are caused by pyogenic bacteria, in immune compromised, some may be fungal or mixed flora
56
Q

Meningitis

A
  • inflammation of the mennenges
  • viral is most common, and most undiagnosed infectious disease of CNS. Occurs in many diseases such as the common flu
  • characterized by lymphocytic exudate in the subarachnoid space
  • viral encephalitis may also extend into the menenges, which would show lymphocytosis and increased protein in CSF
  • bacterial menengitis (S.pneumoniae, and N. Meningitisis), characterized by an exudation of neutrophils. In severe cases, entire surface brain is covered in pus that fills the subarachnoid spaces. Numerious neutrophils in CSF -nb for establishing dx. Glucose in CSF is low, due to being consumed by bacteria
57
Q

Neurosyphilis

A
  • presents as chronic meningitis
  • meneges are infiltrated with lyphocytes and plasma cells, which are centered on small blood vessels
  • in healing phases, menengeal firbrosis predominates
  • fibrosis of menenges may compress doral roots, which may result in atrophy of afferet, sensory axons entering the spinal cord. This causes the best known complication of syphilis= tabes dorsalis
  • Tabes dorsalis is recognised on cross section of the spinal cord as atrophy of the dorsal columns (sensory)
  • perivascular inflammation of the brain imparis blood flow and causes ichemic necrosis of the cortical centers
  • loss of neurons= mental and deteriation =syphilis general paresis of the insane
58
Q

Aids related encaphalopathy

A
  • common finding in terminal aids
  • hiv infects the t-lyphocytes and macrophares -bringing the virus into the CNS. They secrete cytokines which are toxic to brain cells. Results in aids dementia
  • aids infected brain is less resistant to pathogens. Most prominent are toxoplasma and cryptococcus. Menengitis, encephalitis, or brain abcess may develop. most of these are resistant to tx., thus many die of CNS infection.
59
Q

MS

A
  • demylenating disease of autoimmune origin
  • most common immunologic CNS disease
  • 20-45 years of age
  • prevalence is 1:1000, leading neurologic disease in young adults
  • twice more common in women
  • symptoms occur at any age but rarely before puberty and after 50
60
Q

Etiology of MS

A
  • cause is unknown
  • occurs more often in whites in western or northern european origin, less in tropics
  • genetic studies show it affects some families more than others
  • person with 1st degree relative has 15% higher risk
61
Q

Pathogenesis of MS

A
  • mediated by 1.) helper lymphocytes, 2.) macrophages 3.) B-Cells and plasma cells
  • p.481
62
Q

Pathology of MS

A
  • Demylenating disease that typically affects white matter
  • demylenating of axons leads to the formation of plaques that are found in brain, optic nerves, spinal cord
  • periventricular plaques of the lateral hemisphere of the brain is typical
  • early lesions are infiltrated with lymphocytes and macrophages
  • older lesions consist of demylenated axons surrounded by reactice astrocytes
  • Oligodendroglial cells are absent (responsible for mylenation)
63
Q

Clinical Features of MS

A
  • perious of excaserbation and remission of neuro symptoms
  • symptoms include both sensory and motor
  • Sensory: most common is loss of touch, accompanied by tingling. Blurred vision is a common early symptom
  • Motor: muscle weakness, unsteady gait, incoordination of movement, sphyincter abnormalities (incontinence)
64
Q

Diagnosis of MS

A
  • made on clinical grounds
  • documentation of two seperate sets of CNS symptoms that occur in at least 2 episodes, seperated by a period of 1 month or more
  • MRI is useful - brain lesion is evident in 80%
  • Oligoclonal IgG is found in CSF - supports dx.
65
Q

Course of MS

A
  • unpredictable
  • incapacitated in 20-30years
  • pt.s who develop after the age of 40, or with marked motor disability early on have poor prognosis
66
Q

CNS diseases: Inborn errors of metabolism

A
  • Tay Sachs:
  • Neimann Pick
67
Q

Nutritional Diseases of CNS

A

-r/t adequare intake of vitamins

-Thiamine: Presents as Wernicke or Korsakoff.

Wenike: occular, gait, mental function

Korsakoff: menta deterioration (amnesia) and make up incredible stories (confabulation). Degenerative neuronal changes usually found in hypothalamus, midbrain, and mamillary bodies. Both syndromes can be combined.

-VitB12: uncoordinated movements, sensory motor peripheral neuropathy, with signs of spinal cord disease. Typical patients have abormal gait. Some are demented, delerious, depressed or slow.

-Nicotinic Acid Deficiency: results in pellagra (dermatitis, diarhea, and delirium). Neuro and psych symptoms present and hightly variable.

68
Q

Chronic Alcoholims and CNS: direct

A
  • affecs nervous system directly and indirectly
  • damages liver and alter intramediary metabolism. Combined with other nutritional deficiencies (thiamine, folic acid, nicotinic acid)
  • neuropathic changes- reflect complex metabolic and nutritional
  • pathologic lesions located in same regions as midbrain as thiamine deficiency
  • cerebellar atrophy: uncoordinated walking
  • general cortical atrophy: progressive mental deterioration, loss of memory, inability to concentrate, irritability
  • myelopahty and sensory -motor neuropthy account for sensory deficiencies
  • direct adverse affect of straited muscle
69
Q

Indirect damage with alcoholism

A
  • subdural hematoma
  • DT
  • pontine mylenolysis: lesion in the pons r/t sodium and water imbalance r/t cirrhosis
70
Q

Degenerative Diseases: Image

A
71
Q

Alzheimers Disease

A
  • dementia of unknown etiology
  • characterized by atrophy of the frontal and temporal cortex
  • 70yo and older, rarely younger than 60
  • genetics: chromosome 21 and 19
    p. 484
72
Q

Diagnosis of Alzheimers

A
  • based on gross and microscopic neuropathologic findings
  • Brain appears atrophic and shows narrowing of giri and widening of sulci

Atrophy: prominent is frontal and temporal lobes

Histologic changs most prominent in the cortex. Features or neuritic plaques, neurofibrillary tangles, degeneration, deposition of amyloid in neurogenic plaques and wall of cerebral vessels

73
Q

Clincal Features of Alzheimers

A
  • present with dementia: progressive loss of cognitive function and functional decline that interferes with work and social activities
  • loss of memory predominates, progresses until completely disfunctional
  • most also develop speech problems, must limit their activities, and eventually become bed ridden
  • death r/t decreased resistance to infection
74
Q

Clinical Dx. of Alzheimers

A
  • based on demonstration of progressive dementia
  • dx. made after excluding other causes
  • xray not diagnostic, since atrophy can develop by other means
75
Q

Parkinsons Disease

What kind of disorder?

Characterized by

how common?

what age group?

A
  • subcortical neurodegenerative disorder
  • characterized by movement disorders and pathologic changes of the extrapyramidial (involuntary) motor systems of the midbrain
  • relatively common
  • affects elderly
76
Q

Etiology and pathogenesis of Parkinsons

A
  • Etiology is unknown
  • decreased number of dopaminergic neurons in the substancia nigra. These release dopamine.
  • the striatum and substancia nigra form a functional unit
  • The S.Nigra is depigmented b/c of loss of pigmented neurons. Dopamine in striatum is reduced
  • loss of neurtransmitters- clinical appearance of movement disoders
  • the midbrain centers coordinate these movements and the impulses essential
  • L-dopa may help, but most disease is progressive
  • most patients have idiopathic form
77
Q

Clinical features of Parkinsons

A
  • PD presents with movement distrubances: shaking, rigidity, bradykinesia,
  • significant depressed, 10% dementia
  • no cure, tx. is symptomatic
78
Q

Pathology of Parkinsons

A
  • striatonigral part of the brainstem
  • s.nigira appears pale
  • presnece of lewy bodies: composed of beta-synuclein (a protein in familial PD), fillaments, ubiquitin, and parkin. Contributes to depression and dementia
79
Q

Huntingtons

A
  • rare autosomal dominant neurogenerative disease, affecting striatal neurons but also cerebral cortex
  • clinically presents with motor disturbances, progressive dementia, and abnormal behavior.
  • Familial, 1:20,000
80
Q

Pathogenesis of huntingtons

A
  • gene on chromasome 4
  • CAG trinucleotide repeat, appears at an earlier age and is more severe with each generation
  • characterized by atrophy and loss of nerve cells in the caudate and putamen, accompanied by a variable atrophy of motor corex of frontal lobe
81
Q

Clinical Feature of Huntingtons

A

-symptoms begin by age of 40, 10% dx. as children

Adults: symptoms include involuntary, gyrating movements of the trunk and limbs, postural instability, rigidity, progressive dementia

Children: Bradykinesia, rigidity

-rapid onset when symtoms appear, by 20 years after onset pts become incapacitated and die

82
Q

What is ALS

A

-rare neurodegenerative disease characterized by motor weakness, and progressive wasting of muscles in the extremities, leading ultimately to generalized muscle loss and death

83
Q

Etiology and Pathogenesis of ALS

A
  • cause is unknwon
  • familial form, 10%, linked to copper zinc something on chromosome 21. That this mutation deprives neurons protection from superoxide
84
Q

Pathology of ALS

A
  • loss of motor neurons in spinal cord, midbrain, and cerebral cortex
  • most prominent is the loss of lateral cerebrospinal pathways in the spinal cord, and lateral parts of white matter are replaced by sclerosis
  • this change r/t loss of motor axons and skeletal muscle atrophy is seen on muscle biopsy
85
Q

Clinical Features of ALS

A
  • Usually older men and women
  • presents with weakening and wasting of small hand muscles
  • fasciculation (involuntary muscle twitching). fast involuntary contractions, that do not move the limbs
  • speech becomes slurred, and in advanced cases, but intellect is not affected
  • ultimtely die of paralysis of resp. muscles
86
Q

Dx. ALS

A
  • made clinically
  • electromyography shows denervation and muscular atrophy
  • progressive, leads to death in a few years
87
Q

Epilepsy

A

-group of diseases that present with recurrent seizures. Typically characterized by convulsions, may have short periods of altered conciousness, altered sensory, inapropriate behavior

88
Q

Etiology and Pathogenesis of Epilepsy

A
  • result from focal or generalized dysfunction of the neurons in the cerebral cortex, as a result of neurologic or systemic disease
  • most cases, cause is not known (idiopathic), begin in childhood ages 2-15, presumptive genetic cause.
  • Secondary Seizures: drugs, CNS infection, trauma, tumors

-

89
Q

2 types of Epilepsy

A
  • Focal
  • generalized
90
Q

Generalized Epilepsy

A
  • in most instances, idiopathic and occurs in childhood
  • risk is 1%
  • cause is not known, no associated with pathologic
  • clinically presents with generalized seizures, resulting from bilateral diffuse electric discharges involving the entire cerebral cortex
  • convulsions are tonic-clonic, person usually loses conciousness
  • may be preceeded by an aura
  • after the attack, post-ictal phase
91
Q

Focal Epilepsy

A
  • electrical discharges originate from a well defined cortical area
  • may remain localized or spread
  • can occur at any age, and linked to a defined event ex. infection
  • In children: developmental abnormalities and infection

Adults: trauma or infections. Is first sign of a brain tumor

92
Q

Dx. of epilepsy

A
  • based on clinical data, EEG recordings
  • must distinguish between idiopathic and secondary
  • drug therapy eliminates in 1/3
  • most patients with idiopathic lead a normal life
93
Q

CNS Neoplasms

A
  • Rare, account for only 2% of cancer deaths
  • brain tumors have very high mortality rate
  • brain tumors can occur at any age, but more prominently in younger. In childhood brain ca accounts for 20% of malignant disease.
  • in age 20-40s still most common cancers, accounting for 10% of cancer deaths
  • 50% are primary, 50% are mets
  • intracranial tumors classified as benign or malignant
  • malignant in brain do not metastasize
94
Q

Brain Ca: death from

A

-intracranial mass effect and compression of vital centers. Can be direct compression, or increased ICP and compression of brainstem by herniated cerebellar tonsils, or uncal gyri of the hippocampus

95
Q

Etiology and pathogenesis of brain tumors

A

-cause unknown, no definitive risk factors

96
Q

What are Gliomas

A
  • tumors arising from glial cells.
  • Can be classified as astrocytic, oligodendroglial, ependymal
97
Q

Astrocytic Tumors

A
  • known as astrocytomas, or glioblastomas, account for 80%
  • can be divided into 2 groups:

non-infiltrating: pylociti astrocytomas. Well circumscribed tumors that often occur in cerebellum of children and young adults. Located in floor of 3rd ventricle and in cerebral hemispheres.

infiltrating astrocytomas: most common brain tumors, account for 80% of all intracerebral tumors. Classified into 3 groups: diffuse astrocytoma, anaplastic astrocytoma, and glioblastoma. These infiltrate, and destroy the brain causing hemmorhage and necrosis.

98
Q

Glioblastoma

A
  • most common CNS tumor
  • peak incidence at 65
  • most found in lateral hemisphere of the brain
  • has highly variegated, gross appearance
  • parts are necrotic yellow, parts are hemmorhagic
  • irregular shape, poorly demarkated, often extending from one hemisphere to the other- butterfly like appearance
99
Q

Oligodendrogliomas

A
  • rare
  • involves cerebral hemisphere of middle aged adults
  • partically cystic and calcified
100
Q

Ependymomas

A

p.489

101
Q

Meduloblastoma

A
  • cerebellar childhood tumor of uncertain origin
  • assumed that it arises from fetal neural cell precursors
102
Q

Meningioma

A
  • arise from the menenges
  • most are benign, 4% are malignant
  • located in the midline, from outside the cerebral hemispheres
  • can also arise from the base of the brain
  • spinal meningiomas 10x more common in women
  • compression may cause seizure or motor deficits
  • most are surgically curable with excellent prognosis
103
Q

Which cancers like to metastasize to the brain

A

-lung, breast, melanoma

104
Q

Nerve Sheath Tumors of cranial and spinal nerves

A

Nerve sheath tumor: neuromas

  • originate from schwann cells=schwannomas
  • originate from neurofibroblasts: neuromas
    p. 490
105
Q

Cancers with prediliction for the brain

A

breast, lung, and melanoma

any part of the brain may be involved