The Aging Healthfully Virtual Library
- The Works of Majid Ali, M.D.
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INTEGRATIVE MEDICINE
Majid Ali, M.D.
Course Description, Goals, Objectives, and Related Information
INTEGRATIVE MEDICINE SEMINAR/PRACTICUM - #19
Majid Ali, M.D.
Subject: Disorders of the Brain
Case # 1
In the spring of 1997, a 31-year-old woman presented with disabling
chronic fatigue of 4-year duration which developed after a highly stressful personal
circumstances. She was an active, healthy teenager. Her menarche was at 15, and her
menstrual cycles were regular during the first few years. She was prescribed an oral
contraceptive (exact type unknown to the patient) for severe PMS after a negative
laparoscopy for suspected endometriosis. In 1994, one year after the onset of disabling
fatigue, she developed speech difficulty, facial numbness, and muscle stiffness one week
after receiving dental braces. Her neurologic symptoms subsided 6 weeks later. An MRI scan
of the head in 1994 showed early demyelinating lesions. She discontinued wearing he braces
5 months later and remained free of symptom for one year. Her personal life became highly
stressful again. Her neurologic symptoms recurred after dental "bleaching." At
that she also developed bladder control difficulties. She consulted two neurologists who
prescribed variously neurontin, carbamazapine, betaserone and interon at different times.
Repeat MRI scans in 1995 and 1996 showed persistence of demyelinating lesions.
Notwithstanding multiple attempts to control her progressive neurologic symptoms with
drugs, her general condition deteriorated to a point that walking became very difficult,
and had frequent falls. Other pertinent features of her past history included recurrent
episodes of sinusitis, chronic constipation, dizzy spells, and cognitive difficulties.
Soon after her cycles became irregular, occurring every five to seven months, with some
periods of amenorrhea.
The pertinent laboratory data included the following: WBC, 5800; Hb, 15
g/dL; estradiol, 46.45 pg/mL; FSH, 3.6 mU/mL; LH, 5.7 mU/mL; prolactin, 5.3 ng/mL (all
hormones values represent 12th day of the cycle); testosterone, 53 ng/dL; serum potassium,
3.2 mEq/L; ALT, 56 IU/L; PLF, 3+; (1+ four months after beginning the program);
antinuclear and lyme antibodies, negative; T4, 6.7 ug/dL; T3 uptake, 1.02 uptake units;
TSH, 1.12 uU/mL; cobalamine, 714 pg/mL; ferritin, 60.55 ng/mL; folate, 10.7 ng/mL;
A 24-hour urinary steroid analysis revealed markedly low to
nondetectable values of several metabolites. The table included below shows the steroid
profile before and eight months after beginning an integrative plan.
Case # 2
In summer of 1992, a 46-year-old engineer came to the Institute in a
wheel chair. He had a near total loss of muscle power in left arm and progressive muscular
weakness of right arm and legs. His health had been generally very good until 15 months
prior to the onset of his illness. He had been athletic, traveled extensively for his
company, and lived an active life with his wife and two children before his illness.
Muscles of both arms, hands, legs and feet showed moderate to advanced changes of muscle
atrophy. His mentation was well preserved. The examination of the had and neck and
abdominal visceral was not remarkable.
Questions for case 1 and 2
1. What are the differential diagnoses in case 1?
2. What are the differential diagnoses in case 2?
3. What is demyelination? Is it reversible?
4. How is the anterior horn cell disease diagnosed?
5. What are the salient histopathologic changes observed at autopsy when
patients succumb to
diffuse demyelination in the brain?
6. What are the salient histopathologic changes observed in the brain at
autopsy when
patients succumb to cerebral arterial
thrombosis?
7. What are the salient histopathologic changes observed in the spinal
cord at autopsy when
patients succumb to anterior horn cell
degeneration?
8. How detailed should be the study of an integrative physician of
pathologic lesions in the above
two disorders?
9. The patient in case 2 was enrolled in a drug trial for sixteen weeks.
He reported that he was the
only patient in a group of 13 patients
he responded positively to the drug, though for a period of
some weeks. He asks you if EDTA
chelation that he received during that time might have
something to do with that. How would you
respond to him?
10. What prognosis would you offer to the patient in case 1?
11. What prognosis would you offer to the patient in case 2?
12. Write an integrative management plan for case 1.
13. Write an integrative management plan for case 2.
Clinical Management and Outcome of Case One
A comprehensive integrative management plan was instituted that focused
on vigorous mesaures for restoring her bowel ecology, controlling oxidative coagulopathy,
and hepatic detoxification. Her intravenous therapies included the following: 23 hydrogen
peroxide infusions, each with an intramuscular injection ( IM 6 or IM5 on alternate
basis); 7 fatigue IV infusions; and 18 EDTA chelation infusions. About eight months later,
a program to slowly and safely removal of all her dental mercury fillings (including EDTA
chelations on the day of removing fillings) was implemented. About eighteen months after
she was first seen, she reported a "near complete" control of her neurologic
symptoms and disabling fatigue. Her premenstrual symptoms were markedly reduced and her
menstruation approached a monthly cycle.
During the summer of 1999, she travelled extensively in Russia and
France for three weeks and returned with a full-blown relapse of her original symptoms of
muscle spasm and difficulties of speech, balance, and bladder control. Again, she was put
on an aggressive integrative plan with two IV infusions a week, and vigorous mesaures for
restoring her bowel ecology, controlling oxidative coagulopathy, and hepatic
detoxification. Within seven weeks, she became symptomfree and remained so until early
2000 when she conceived. In the fall of that year, she delivered a healthy baby.
Clinical Management and Outcome of Case Two
A comprehensive integrative management plan was instituted that focused
on vigorous mesaures for restoring her bowel ecology, controlling oxidative coagulopathy,
and hepatic detoxification. Her intravenous therapies included the following: 12 hydrogen
peroxide infusions, each with an intramuscular injection ( IM 6 or IM5 on alternate
basis); 21 EDTA chelation infusions.
The general condition seemed to improve during the initial months of
treatment. However, no clear improvement in neurological symptoms was seen. He became
progressively weak and in several months lost the use of his right arm. Further
deterioration involved swallowing and breathing muscles. He died after two years after he
was initially seen.
Case # 3
A 73-year-old man consults you for a stroke which left him with
weakness of left side of the face, left arm, and left leg.
Questions for case 3
1. What are the differential diagnoses in case 3?
2. What changes in tendon reflexes would you expect?
3. What is encephalomalacia?
4. What is cerebral infarction?
5. What is cerebral ischemia?
6. What is reactive gliosis?
7. How do you clinically differentiate between cerebral hemorrhage and
thrombosis?
8. Which one generally carries a better prognosis, cerebral hemorrhage or
cerebral thrombosis?
9. What prognosis would you offer the patient if he came to you within 24
hours of his illness?
10. What prognosis would you offer the patient if he came to you within 7 days of his
illness?
11. What prognosis would you offer the patient if he came to you after six months of his
illness?
12. Would you recommend growth hormone for this patient? If so, why?
13. Write an integrative management plan for the patient in case 3.
NEURONAL INJURY AND REPAIR
Patterns of Neuronal Injury
Neurones are cells located in the gray matter and are either aggregated
in nuclei, in layers as in six-layered cerebral cortex, or in columns. Neuronal reactions
to injury occur as: (1) axonal reaction, after the axon is cut or otherwise injured,
represents a healing response characterized by rounding and enlargement of the cell,
enlargement of the nucleus, and dispersion of the Nissl substance; (2) acute cell necrosis
(red neurone) due to anoxia or dysoxygenosis; (3) atrophy of cells surrounded by areas of
gliosis (proliferation of the connective tissue of the brain parenchyma); (4) neuronal
degeneration surrounded by areas of gliosis; and (5) accumulation of oxidized and
denatured lipid, protein, and carbohydrate complexes (i.e., lipofuscin) indicating mild
degenerative changes associated with aging.
Patterns of Glial Reactions
Glia is the stroma (the connective tissue scaffolding) of the brain
parenchyma. It includes four types of cells: (1) astrocytes are large cells with round to
ova nuclei; (2) oligodendrocytes are smaller denser cells; (3) ependymal cells are
columnar in shape, have ciliate borders, and line the inner surfaces of ventricles; and
(4) microglial cells that are elongated and contain irregular nuclei.
In neuropathology and neurology texts, glia is delegated a largely
structurally supportive role with participation in repair reactions. In my view, such
thinking is very limited and is wholly inconsistent with the profound regulatory roles of
the matrix in other tissues. In my view, glia asserts foundational regulatory roles in
health as well as in all pathophysiologic phenomena affecting the brain parenchyma. Though
at this time I base my view largely on the many established roles of matrix in other
tissues. It seems safe to predict that future research will clearly show that to be the
case.
Patterns of Neuronal Regeneration
Until recently, the prevailing belief in neurology was that human
neuronal death results in permanent loss of the function of those cells. Indeed, of all
the body's cells, neurones seem least capable of repair and regeneration when injured by
neurotoxins, infectious diseases, stroke, or degenerative disorders. A spate of recent
studies have clearly demonstrated the ability of neurones to regenerate. Still, neurones
of neocortex—the region of the brain of greatest interest from the standpoint of
functions involving mood, memory, and mentation—appeared not to participate in repair
and regenerative functions. Now that also is changing. Consider the following:
"...when they induced certain neurones in the neocortex of adult
mice to self-destruct, the loss triggered the formation of replacement neurons by brain
stem cells. What's more, the newly formed neurones migrated to the same position as their
deceased predecessors."
In the experimental cited above, opoptosis of neocortex cells was
selectively induced with light-activated compound. The death of neocortical cells then
triggered the multipotential neural precursor (stem) cells located in the subventricular
zones to produce new neurons which then traveled to find their home in the area of dead
cells and replaced them. The tracking of the new neurons was done by labeling those cells
with a tracer chemical (5- bromodeoxyuridine). Further experiments with a dye demonstrated
that the newly formed neocortical cells established the same functional axon connections
to thalamus as the original cells.
1. Lasley EN. Death leads to brain neuron birth. Science
2000;288:2111-2.
2. Magavi S, Leavit B, Macklis J. Nature June 22, 2000
Oxidative-Dysoxygenative Perspective on Neuronal Injury and Repair
The brain parenchyma is a highly aerobic tissue and yet does not hold
any oxygen reserve. The brain draws about 15% of the resting cardiac output and 20% of the
total body consumption of oxygen. Unlike in many other body tissues, oxygen availability
is the rate-limiting factor in brain metabolism. For those reasons, neuronal metabolism
begins to be impaired within 8 to 10 seconds of oxygen deficiency and irreversible damage
occurs within 6 to 8 minutes. By contrast, neuronal glucose reserves can maintain
metabolism for 30 to 60 minutes after glucose supply is turned off. Hence, even severe
hypoglycemia in most clinical situations can be effectively managed without irreversible
neuronal injury.
In my view, the molecular underpinnings of all types of toxic,
metabolic, ischemic, degenerative, and infectious injuries to brain parenchyma involve
oxidative-dysoxygenative phenomena. I draw this conclusion from the examination of
experimental and clinical observations reported about the various clinicopathologic
entities concerning the central nervous system. For example, the the genetic locus on
chromosome 21 in familial AML appears to be the Cu/Zn-binding superoxide dismutase.
Monoamine oxidase inhibitors are of limited benefits in the early stages. As for the
common stroke, Alzheimer's disease, and heavy metal toxicity, the oxidative-dysoxygenative
nature of the nature is self-evident. From the standpoint of integrative medicine, this is
of paramount importance since it means all effective integrative therapies for brain
disorders must be sharply focused on issues of oxidosis and dysoxygenosis.1
1. Ali M. Darwin, oxidosis, dysoxygenosis, and integration. J
Integrative Medicine 1999;3:11-16.
Perinatal Brain Injury
Cerebral palsy is an inclusive descriptive term for all forms of
nonprogressive motor deficit of neurologic origin that develop during the perinatal
period. It does not connote any etiologic factors. Some such cases are due to hemorrhage
in the brain parenchyma, the region between the thalamus and cuadate nucleus being often
involved. In other cases, microinfarcts occur in the periventricular white matter
(periventricular leukomalacia). The cranium has very limited expansible capacity.
BRAIN EDEMA
The cranium has very limited expansible capacity. Furthermore, the
brain has few, if any, demonstrable functioning lymphatic channels under ordinary
conditions. Thus, the presence of very small amounts of excess fluid puts into serious
jeopardy the physiologic as well as compensatory pathophysiologic processes. The junctions
between the capillary endothelial cells and glial surfaces are tight and closely regulate
the to and fro movement of fluid and solutes between the two compartments. That is the
morphologic underpinning of the brain-blood barrier (BBB).
Cerebral edema is of three main types: (1) vasogenic due to changes in
permeability; (2) cytotoxic due to intracellular and extracellular fluid regulations; and
(3) interstitial edema that is regarded as transudate. All three types occur in acute
oxidative-dysoxygenative lesions associated with infectious, toxic reactions, metabolic
derangement, and malignant neoplasms.
As in the case of the pathophysiologic roles of the glia, there are
major differences in the prevailing opinions in neurology and neuropathology on one hand
and integrative medicine on the other. I believe cerebral edema plays a significant
contributory role in the pathogenesis of many neurologic symptoms seen in
fatigue/fibromyalgia complex and those associated with allergic reactions, chemical
sensitivity syndrome, and environmental exposures as well as in hormone disorders, such as
severe PMS, endometriosis, and others. The concept of brain allergy usually draws
derogatory comments from most neurologists. Yet, it is a valid concept from a clinical
standpoint since it calls for detox measures and the use of diuretics to control symptoms.
CEREBRAL ISCHEMIA AND INFARCTION
The common term stroke refers to loss of neurologic function caused by
death of brain cells due to hemorrhagic infarction (cerebral hemorrhage) or ischemic
infarction (cerebral thrombosis). The term TIA (transient ischemic attacks) refers to
temporary loss of some brain functions due to reversible ischemia, often caused by a spasm
of cerebral arteries.
Causes of Brain Hypoxia and Anoxia
1. Functional hypoxia due to diminished partial pressure of oxygen (pO
2) in the inspired air.
2. Severe hypoxia due to generalized cardiovascular failure, such as in
cardiac arrest.
3. Impaired oxygen carrying capacity due to anemia.
4. Impaired oxygen carrying capacity due to toxins, such as carbon
monoxide.
5. Temporary perfusion deficits caused by vasospasm.
6. Long-lasting perfusion deficits caused by vascular occlusion.
7. Inhibition of oxygen metabolism by poisons, such as arsenic.
8. Dysoxygenosis (inhibition of oxygen metabolism by impaired function
of oxygen metabolism due
to cumulative burden of environmental
and microbial toxins as well as toxic organic acids
produced in excess due to acidosis and
oxidosis).
Two important molecular pathways in anoxic and dysoxygenetic brain
injury are noteworthy. In the first, initial oxygen deficiency leads to overproduction of
certain excitatory amino acid neurotransmitters (including glutamate and aspartate). That,
in turn, seriously threatens the neuronal metabolism by further reducing oxygen supply.
The putative mechanism of such injury involves persistent opening of such specific
membrane channels as NMDA (N-methyl-D- aspartate receptor) that maintains uncontrolled and
dangerous influx of calcium ions. Increased intracellular calcium promotes cell apoptosis
in addition to exert other cytotoxic effects.
The second mechanism of incremental neuronal injury involves activation
of nitric oxygenase, an enzyme that plays crucial regulatory roles in health by carefully
controlling the production of nitric acid, another important neurotransmitter and a highly
potent toxin when present in excess.
Ischemic Encephalopathy
very mild forms of ischemic encephalopathy may cause short periods of
mental confusion with full recovery. In moderate cases, there is progressive impairment of
mentation which, unless expeditiously reversed, leads to permanent functional loss. In
severe cases, extensive necrosis of brain parenchyma leads to diffuse softening of the
brain parenchyma so that brain tissue becomes diffluent and freely flows through fingers
when the brain is pulled out of the skull at autopsy.
Cerebral Infarction
Discrete areas of brain necrosis (infaction) usually result from:
1. Thrombotic occlusion due to arteriosclerosis developing within the
brain.
2. Embolic occlusion due to emboli formed outside the brain and carried
in there
(as in atrial fibrillation).
3. Cerebral hemorrhage due to leaking or rupture of blood vessels, as in
malignant
hypertension (lacunar state) and
aneurysm blow-outs.
4. Trauma.
5. Hemorrhage in neoplasia.
6. Septicemia.
About 15% of cases of cerebral hemorrhage die with or without
treatment.
DEMYELINATING DISORDERS
are characterized by damage to myelin sheath while the axon structure
and function is relatively preserved (at least in the early stages), and include the
following:
1. Multiple sclerosis
2. Neuromyelitis optica (Devic's disease), mostly in Asians
3. Acute disseminated encephalomyelitis (ADEM)
4. Central pontine myelinolysis (thought to be related to rapid
correction of hyponatremia)
Multiple Sclerosis (MS)
is the most common demyelinating disorders, and is an intermittent
disorder characterized by episodes of neurologic deficits associated with discrete and
noncontiguous demyelinating lesions of the white matter. In MRI scans, such lesions appear
as "white" lesions. Most MS patients show monoclonal bands of proteins in
cerebrospinal fluid specimens. There are known associations with several MHC antigens,
including A3, B7, DR2, Dqwl, DQB1, and DQA1. Some reports point to polymorphims involving
the alpha and beta subunits of the T-cell receptors. Both CD4+ and CD8+ lymphocytes are
present in MS lesions.
The incidence of MS is 1 per 1000 persons in the United States and
Europe and in, general, increases with distance from the equator. After migration, people
take on the risk of the new geographic region.
I believe MS is largely a disease produced by mycotoxicity, with heavy
metal and other types of toxicities playing secondary roles.
I base my opinion not only on the known geographical distribution of
the disease but also on my observation that persons living in true desert environment
(where there are no mold overgrowth) do not commonly suffer from MS.
AMYOTROPHIC LATERAL SCLEROSIS
(ALS, Lou Gehrig's Disease)
ALS is a very serious and a specific type of neuronal degeneratory
disorder characterized by loss of lower and upper motor neurons. Muscular atrophy,
weakness, and fasiculations result from the injury to the former while muscle spasticity,
hyperreflexia, and positive Babinski sign appear due to involvement of the former.
Approximately 10% of cases seem to be familial. The genetic locus on chromosome 21 in such
cases appears to be the Cu/Zn-binding superoxide dismutase.
In the nonfamilail types, a high prevalence of HLA-A3 and B12
haplotypes points to an underlying oxidative- immune diathesis. In animal studies, some
plant-derived neurotoxins produced an ALT-like state.
I have observed limited clinical results with antioxidant and
oxygenative therapies supported by strong bowel, blood, and liver detox measures.
ALZHEIMER"S DISEASE (AD)
AD is an insidious and a progressive disorder of intellectual
impairment and changes in mood and memory. Severe cortical dysfunction can lead to a
immobility and mutism. The incidence rises from the fifth decade of life steadily so that
about 20% of persons over 75 years of age and 50% of those over 85 suffer from it. Five to
ten percent of cases are thought to be familial in nature.
The salient gross pathologic changes include diffuse cortical atrophy
with widened sulci and
enlargement of ventricles. The major
microscopic changes include:
a. Nurofibrillary tangles (bundles of basophilic filaments within the
neuronal cytoplasm that displace
the nucleus) and loss of neurones.
b. Neuritic (senile) plaques are composed of dystrophic neurites.
c. Amyloid angiopathy involving deposition in the vessel walls of
amyloid beta peptide.
Considerable direct and indirect evidence points to the involvement of
amyloid beta peptide and its precursor protein called APP in the pathogenesis of AD. APP
has a large extracellular domain, a membrane-spanning region, and a short intracellular
domain. Point mutations in genes coding APP have been identified. Under physiologic
conditions, processing of APP includes cleavage of beta peptide to prevent production of
insoluble aggregates of mcromolecules that trigger the formation of amyloid material as
well as neurofibrillary tangles.
In 1995, I proposed a hypothesis that AD results from oxidative injury
to proteins as well as lipid and glycolipids in the brain parenchyma. Specifically, I hold
that AD is essentially caused by oxidative injury to beta peptide and APP. Of considerable
interest in the context is role of oxidative coagulopathy in pathogenesis of AD. Some
isoforms of APP containing a domain called KPI (Kunitz protease domain) that exert
regulatory influence in clotting cascades.
Oxidative Theory of Alzheimer's Disease
The following text reproduced from RDA: Rats, Drugs and Assumption
(1995) may be of some general interest to the reader.
Abnormal, oxidatively damaged proteins called beta-amyloid proteins
occur in the brains of people who suffer from Alzheimer's disease. The tangled fibers made
up of such proteins literally choke the neurons and nerve fibers trapped in them. Such
telltale signs of cell death are called neurofibrillary tangles or plaques. Four years
ago, Yankner and co-investigators at Harvard Medical School published an important paper
showing that beta-amyloid proteins indeed are toxic to nerve cells. Predictably, that
report triggered a flurry of activity in the drug industry to develop drugs that inhibit
plaque formation in the brain and prevent Alzheimer's disease. There were the expected
pronouncements of an imminent drug breakthrough for this dreadful disorder.
No one bothered to ask the basic question: If Alzheimer plaques are
caused by oxidatively damaged proteins, why would any drug for this disease fare any
better than thousands of other drugs that have failed miserably for other oxidative
degenerative disorders in the past?
Alzheimer's disease is a dreaded disorder that causes memory loss and
dementia. This disease has a very strong link with high aluminum content of the brain
tissue. The overload of neurotoxic metals such as mercury, lead, nickel and others can be
fully expected to add to the injury caused by aluminum. Most people with Alzheimer's
disease also show evidence of poor circulation due to plaque formation in the brain blood
vessels. In view of these considerations, what therapy can be expected to be most
beneficial for patients with Alzheimer's disease? A therapy that takes toxic metals out of
the brain tissue and a therapy that improves the blood circulation to the brain. What
therapy eminently accomplishes both goals? EDTA chelation therapy. Oops! Those chelation
quacks again!
Is beta amyloid protein found in plaques of Alzheimer's disease a
product of oxidative damage to natural proteins present in the brain? Objective scientific
evidence for this has not yet been published. So it remains speculative on my part at this
time. However, I have absolutely no doubt that such evidence will be forthcoming with
future research in this area.
The disease doctors of drug medicine do have a problem. When proteins
are oxidatively damaged, they cannot be "un-oxidized" by drugs to undo the
tissue damage caused by them. The only real chance we have of reversing such lesions is to
prevent further oxidative damage and to facilitate recovery using Nature's own way of
replacing oxidatively damaged proteins with newly synthesized, unoxidized proteins. The
problem for drug doctors is that such a philosophic approach is considered unscientific
and so unworthy of the scientists at the National Institutes of Medicine (NIH). Why?
Because quacks were there first. The NIH syndrome thrives in our universities.
PARKINSONISM
is a clinical syndrome of flat facial affect (diminished expression),
sluggish movements, stooped posture , and festinating gait (a "shuffling" walk
with progressively shortened, accelerated steps). Following are principle entities
included in Parkinsonism:
1. Idiopathic Parkinson's disease
2. Striatonigral degeneration
3. Shy-Dager syndrome (associated with autonomic dysfunction (oxidative
dysautonomia)
with orthostatic hypotension).
4. Progressive supranuclear palsy
5. Drug-induced Parkinsonism, especially methyl phenyl
tetrahydropyridine (MPTP) produced
as a byproduct in illicit production of
meperidine analogues
6. Postencephaltic Parkinsonism
The common pathogenetic mechanism in all involves injury to
nigrostriatal dopaminergic system. Pathological features include pallor and depigmentation
of substantia nigra and locus ceruleus. Histologically, there is loss of pigmented
catecholaminergic neurons, gliosis, and presence in neurons of bright eosinophilic Lewy
bodies.
Monoamine oxidase inhibitors are of limited benefits in the early
stages. Stereotactic implants of fetal mesencephalic tissue into the striatum show some
promise. Fetal cell injections with implants into the striatum tissue are also sometimes
helpful for variable periods of time. Aggressive integrative detox, nutrient, and
chelation therapy in early to moderate cases appear to give the best results.
Pick's Disease
Less common than Alzheimer's disease, Pick's disease also causes severe
dementia and often runs a similarly devastating clinical course. Pathologically, it is
distinguished from Alzheimer's disease by the presence of "lobar atrophy"
causing asymmetrical atrophy of frontal and temporal lobes and generally sparing the
parietal and occipital lobes. Microscopically, there is severe neuronal loss. Some
surviving cells are markedly swollen (Pick cells) and may contain eosinophilic bodies
(Pick bodies).
General Questions
1. Drilling of the occipital bone to relieve Budd-Chiari compression in
fibromyalgia should
not be unnecessarily deferred when indicated.
F
2. The differential diagnoses of multiple sclerosis must include Lou Gehrig's disease. F
3. Deep tendon reflexes are increased in areas affected by encephalomalacia. F
4. Deep tendon reflexes are increased in areas affected by cerebral hemorrhage. T
5. Cerebral infarction and cerebral ischemia are synonymous terms. F
6. Reactive gliosis is scarring in the brain parenchyma. T
7. Clinically differentiation between
cerebral hemorrhage and thrombosis is
sometimes extremely difficult. T
8. Ventricles in Alzheimer's disease usually show contraction. F
9. Neurofibrillary tangles are pathognomic of Alzheimer's disease. F
10. In general, cerebral thrombosis carries a better prognosis than cerebral hemorrhage. T
11. The long-term prognosis of patient with
CVA likely to better if integrative intervention
begins within hours of the stroke. T
12 Growth hormone is beneficial in most patients if administered soon after a CVA occurs. F
13. The neocortex has no demonstrated capacity for regeneration in mammals. F
14. Parkinsonism comprises a spectrum of
clinical disorders with the dominant feature
of memory loss. F
15. A hallmark of clinical diagnosis of
Alzheimer's disease is festinating gait (a "shuffling"
walk with progressively shortened,
accelerated steps). F
16. Anoxia or dysoxygenosis leads to
overproduction of excitatory amino acid neurotransmitters
glutamate and aspartate) which, in turn,
further cause neuronal damage by causing persistent
opening of such specific membrane
channels as NMDA (N-methyl-D-aspartate receptor)
and uncontrolled and dangerous influx of
calcium ions. T
17. Cerebral anoxia decreases the activity of nitric oxidase. F
18. Pick's disease is a clinical syndrome
and pathologically cannot be distinguished from
Alzheimer's disease. F
19. Striatonigral degeneration is common in Alzheimer's disease. T
20. As components of an integrative
management plan, EDTA chelation and large doses of
hydroxycobalamine (in doses of 20 to
30,000 mcg) are often very beneficial in early cases
of Alzheimer's disease. T
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