Disorder

% of endocrine patients with psychiatric symptoms

Symptoms

Thyroid

hyperthyroid

as high as 50%

agitation, depression, schizoid paranoia, hallucinations

hypothyroid (myxedema madness)

as high as 20%

mania, schizoid paranoia, catatonia, depression

Adrenals

90%

some psychiatric disturbances

hyperadrenal-corticolism (Cushing’s Disease)

20 to 30%

depression, delerium, agitated paranoia, hallucinations, suicidal tendencies

hypoadrenalism

60 to 90%

hallucinations, paranoia, catatonia, bizarre posturing – all episodic

Pancreas

hyperglycemia (Diabetes Milletus)

not known

impotence, schizoid depression

hypoglycemia

not known

violence, unprovoked anger, confusion, amnesia

Pituitary

hypopituitarism (Simmonds Disease)

as high as 70%

anorexia, confusion, apathy, depression

1.  Cerebral Atrophy or Sclerosis

The loss of neurons and/or connecting cellular material (e.g. glial cells) of the brain which cause the brain size to shrink and normal processes to cease.

Disease/Condition

Pathology

Psychological Changes

a.  Alzheimer’s Syndrome includes: Kuru, Jacob-Creutzfeld Disease, Alzheimer’s Disease

Familial; slow acting virus a factor in some forms; due to irreversible damage to cerebral outer layers, causing loss of brain cells during middle age.

Cognitive, perceptual motivational and language disturbances.

b.  Amaurotic Familial Idiocy, includes Tay-Sachs, onset 3-4 mo. Old; Bielschowsky, 3-4 yr. old; Nieman-Pick, 3-4 yr. old; Spielmeyer-Vogt, 7-12 yr. old; Kuf’s, adult

Genetic; lipid storage disease with lipid accumulation in cytoplasm of neurons causing them to swell and rupture; the brain becomes small as cells degenerate; due to the absence of an essential lipid-utilizing enzyme.

Listless, sensitive to sound, visual disturbances, mental deterioration (both retardation and psychosis).

c.  Huntington’s Disease

Genetic; insidious onset of cerebral cortical atrophy; disappearance of cells in putamen and caudate nucleus; lateral ventricle enlargement; due to metabolic defect in DNA repair.

May begin with obstinancy and moodiness; lack of initiative; euphoria or spiteful behavior; becomes destructive and violent; paranoid; and final stage is vegetative.

d.  Schilder’s Disease (Sudanophilic cerebral sclerosis)

Unknown cause; occurs in children and young adults; due to demyelination and destruction of cerebral neurons with impeded circulation and excessive development of neuroglia tissue.

Mental deficiencies and personality disorders; progresses more rapidly than multiple sclerosis, which is resembles.

e.  Peligeaus-Merzbacher Disease

Familial; Begins in childhood and progresses for two or three decades until fatal; due to diffuse demyelination of cerebral and cerebellar white matter and brain stem.

Disturbs mentation and produces thought disorders.

f.  Syndeham’s Chorea (St. Vitus’ Dance

Degeneration of neurons in severe cases, in others the damage is not permanent; due to rheumatic fever, lupus erythnatosis, and Schonlein-Henoch (anaphylactoid) purpura; damage mostly in the cerebral cortex and the basal ganglia, especially the striatum.

Uncontrollable awkwardness and facial grimaces with emotional lability and nervousness; occurs most frequently in females under 20 years of age.

g.  Cerebral atrophy

Loss of neurons in brain and subsequent enlargement of ventricles; cause unknown.

Delusional and paranoid behavior; schizophrenic thought disorder.

2.  Cerebral Lesions (tissue damage)

a.  Hemorrhagic and/or Occlusive

Rupture of cerebral blood vessels with interrupted blood flow to related areas of the brain and subsequent compression of brain tissue causing neural dysfunction.  The areas affected may suffer neural necrosis and degeneration, with permanent loss of function and personality disorders.  Occlusion of cerebral arteries deprives neurons of necessary blood flow causing tissue damage or death.

Disease/Condition

Pathology

Psychological Changes

1)  Cerebrovascular Accident (stroke or CVA)

Caused by occlusion of cerebral artery due to thrombosis, embolus, arteriosclerosis; no blood flow permanently or temporarily causing tissue necrosis or damage.

Activity, thought and behavioral abnormalities depend upon area(s) affected by the lesion; emotional instability especially associated with lesions in vertebral or basilar arteries.

2)  Trauma (birth or accidental)

Tissue damage in brain from foreign object or from skull compression; concussion with severity of symptoms depending upon extent of damage to the brain.

See Cerebrovascular Accident

3)  Aneurysm rupture

Congenital or acquired infection can weaken arterial wall causing rupture and hemorrhage.

See Cerebrovascular Accident

4)  Chronic subdural hematoma

Slow or intermittent bleeding from rupture in the vascular bed, usually in the capillaries, with calcification of the clot and pressure on the brain tissue.

Intermittent headache with other neurological signs; patient often labeled neurotic or psychotic because of personality changes and/or memory loss.

5)  Syphilitic lesions

From damage to arterial wall in later stages of the infection.

See Cerebrovascular Accident; Lesions of Infectious Origins.

6)  Emboli

Blood clots or foreign substances which enter cerebral circulation and occlude blood flow, e.g. air emboli, fat emboli, amniotic fluid emboli etc.

See Cerebrovascular Accident.

7)  Korsakoff’s Syndrome

Irreversable damage to cerebral neurons from toxic levels of alcohol over chronic course of alcoholism; also in part from fat embolisms released from the fatty, alcoholic liver and causing repeated small CVA’s in both the cerebellum and cerebrum; thiamine deficiency also a contributing factor to the neural damage.

“Korsakoff’s Psychosis,” with disorientation, memory loss, suggestibility, halluncinations.

b.  Neoplasms (Tumors)

Tumors effect changes in circulation causing compression, distortion and displacement of other structures.  Inter-cranial pressure increases, which interferes with cerebral blood flow and cerebral spinal fluid flow, the latter producing hydrocephalous.  The precise symptoms depend on the location and size of the tumor, but any tumor will eventually affect thought and behavior patterns.

Disease/Condition

Pathology

Psychological Changes

1)  Von Ricklinghausen Disease

Familial; rare; hundreds of neurofibromas and lesions in the CNS and peripheral nerves; onset in childhood.

Symptoms depend upon locations and extent of lesions.

2)  Sarcomas, esp. Giant Cell Fibrosarcoma

Malignant tumor that occurs most often in the temporal lobes.

Temporal lobe lesions usually cause frank psychotic symptoms.

3)  Meningiomas

Tumors of the meninges, or outer covering of the brain and spinal cord.

Associated with depression and other mental changes.

4)  Vascular Lesions

      a)  Lindau’s Disease

Congenital defect that causes multiple hemangiomas of the retina, cerebellum, medulla oblongata, spinal cord and liver; polycystic disease of the pancreas, liver and kidneys; adrenal cortex hyperplasia

See Hyperadrenalism, Hypertension, Fanconi Syndrome.

      b)  Stuge-Weber-         

           Dimitri Disease

Hemangiomas with calcification and iron deposits in the meninges of one hemisphere with port wine hemangioma over the distribution of the trigeminal nerve on the same side or bilaterally; congenital.

See Meningioma

5)  Homen’s Syndrome

Lesion in the lenticular nuclei of the corpus stratum, or gray mass at the base of the ventricles.

Drunken gait, memory loss, confusion progressing due to dementia.

6)  Corpus Caollosum Tumor

Disrupts transmission of impulses between the right and left hemispheres.

Psychotic patterns result from this dysfunction esp. schizophrenic symptoms with depression, delusions and hallucinations if the anterior horn of the corpus colosum is involved.

7)  Frontal Lobe Tumor

Disrupts function of affective and/or cognitive processes depending upon side affected.

Psychotic symptoms may be the first sign of lesion.

8)  Gumma

Soft tumor of tertiary syphilis; develops in the meninges, brain and spinal cord.

See Meningioma.

c.  Infectious Lesions

May be due to many agents, such as viruses, pyogenic organisms, tuberculi bacilli and fungi.  The areas affected may be permanently scarred from neural destruction and cause personality disturbances.

Disease/Condition

Pathology

Psychological Changes

1)  Brain abscess

Permanent destruction of neurons in the area involved, affecting the neural pathways through the areas as well as the processes for which they were designed.

Symptoms depend upon the area involved and the extent of the lesion.

2)  Encephalomyelitis esp. Equine, Eastern virus

Disseminated infection from systemic viral infection such as measles, mumps, etc.  Inflammation of the cerebral cortex, basal ganglia, midbrain and spinal cord with congestion and arteritis.

May have neural degeneration and personality changes.

3)  Encephalitis, Viral esp., St. Louis Herpes, Type-A Lethatgica

Congestion, hemorrhage and necrosis of cerebral cortex and subcortical areas.

May have neural degeneration and personality changes.

4)  Meningitis, esp. chronic forms

      a)  Syphilis

      b)  Tuberculosis

      c)  Cryptococcosis

Cerebral edema with hemorrhage, neural necrosis and degeneration, demyelination; chronic forms often undiagnosed until damage has been extensive and permanent.

Permanent disorders with seizures, behavior and personality changes, hydrocephalus and focal signs of cerebral lesion; early signs often mistaken for psychological problems and treatment is delayed.

5)  Meningoencephalitis

      a)  Mump virus

      b)  Cryptomegalovirus

      c)  Epstein-Barr

           (Mononucleosis)

      d)  Infectious hepatitis

      e)  Acute Multiple               

           Sclerosis

      f)  Herpes simplex

Inflammation of brain and meninges which may have neural necrosis and permanent cerebral disorders.

See Encephalitis, liver dysfunction.

6)  Postencephalitis Parkinsonism

Degenerative lesions of gray matter in brain stem of young adults.

Transient, uncontrollable upward deviation of eyes and personality changes, often progressing to frank psychosis.

7)  Syphilitic meningioencephalitis

A meningitis and arteritis of the brain and spinal cord appearing months to years after infection; inflammatory atrophy of cerebral cortex and overlaying meninges.

Onset insidious with headache, memory and concentration loss.  Personality changes: becomes antisocial and slovenly.  Manic euphoria with delusions of grandeur common.

8)  General paresis (Dementia paralytica)

A type of neuro-syphilis, primarily involving the cerebrum; juvenile form from congenital syphilis appears at about 10 years of age; in adults, 10-15 years after infection.

Atrophy of brain with degeneration of the pyramidal tracts and enlargement of the ventricles; memory loss, megalomania, euphoria, tremors and slurred speech.

d.  Left parietal lobe syndrome

Lesions involving the area of this lobe may be the result of a number of different problems.

Does not recognize or perceive a stimulus and is unable to carry out purposeful movements such as occur with adequate perceptions and normal mental capacity.  Often mistaken for confusion or dementia because behavior can be so inappropriate.

e.  Anoxia

Brain tissue denied oxygen, often secondary to trauma, edema or neoplasms.  Results in cellular death from oxygen deprivation.

See Cerebral Edema, Trauma, Neoplasms.

3.  Structural cerebral anomalies

Inherited or congenital alterations in the size, shape, location and relationship between parts of the brain.  Such alterations result in abnormal processes that often affect perception, affect and cognition.

Disease/Condition

Pathology

Psychological Changes

a.  Klippelfiel Syndrome

Inherited; a reduction in the number of cervical vertebrae and/or fusion of two or more vertebrae, producing a short neck with fluid filled cavities in the spinal cord; results in neural destruction.

Freidreich’s ataxia with impaired speech, spinal curvature, irregular movements and gait; eventual paralysis of lower limbs, mental deficiencies and thought disorders.

b.  Brain asymmetry discordance

Normal brain asymmetry modified during embryonic development with motor dominance not concordant with hemispheric dominance.

Discordance for handedness has been associated with schizophrenic syndrome in which cerebral hemisphere dysfunction is present.

c.  Lateralized dysfunction of anterior limbic system

Fronto-orbito-temporal anterior areas of limbic system have neural disorganization that produces psychotic and epileptic disorders.

Bi-frontal and non-dominant fronto-temporal organization modulates manic-depression dominant side with schizophrenia.

d.  Disorientation of hippocampal pyramidal cells

Genetic or early fetal lesion with disarrangement of these cells so their impulse transmission is affected; changes in substrate of mesolimbic dopamine system.

Schizophrenic syndrome.

e.  Minimal brain dysfunction

Genetic or acquired deficits in brain function that are chronic and sub-clinical; detected only by sensitive neurological testing.

Spatial cognition deficit causes affliction in body image and ego-identity; alterations in perception and problem-solving ability may cause childhood behavior problems; dyslexia from language area deficits; impulse control ineffective because of stimulus barrier.

f.  Hydrocephalus, (normal pressure esp.)

Congenital or acquired from trauma, infection or tumor; cerebrospinal fluid collected in the ventricles, or sometimes outside them, compressing tissue, disrupting neural activity or causing atrophy; head size may remain normal.

With neural pathways interrupted or destroyed in the ventro-medial areas of temporal lobes, (a common area of tissue damage), uncontrollable emotional outbursts may occur.  Also see Seizures, Cerebral Edema.  No response to anti-psychotic medication.

4.  Biochemical cerebral anomalies

Proper function of all brain areas is dependent on neural control of neurotransmitter production, release, degradation or re-uptake.  Disturbances in these processes can produce psychotic thought and behavior patterns.

Disease/Condition

Pathology

Psychological Changes

a.  Neurotransmitter imbalances

These imbalances have been identified primarily in the biogenic amine (dopamine, norepinephrine and serotonin) system with dysfunction of their respective pathways and of the brain areas excited or inhibited by their activity; other neurotransmitters not yet identified may also play a role in psychosis.

Produce both cognitive and affective psychosis depending upon the specific pathway involved.

b.  Briquet’s Syndrome

A somatization disorder with clinical, genetic and prognostic characteristics; the conversion of mental experiences or states to bodily symptoms; a dopaminergic defect.

Shortness of breath and aphonia which are dependent upon hysterical paralysis of the diaphragm and anesthesia of skin and leg muscles.

c.  Gilles de la Tourette Disease

Genetic; increased stimulation of the dopamine pathways connecting the language-emotion areas of the brain; begins in childhood and progresses insidiously to episodes of verbal and gestural responses outside of conscious control.

Patients bark, swear and shout using contorted facial expressions; events occur unpredictably and uncontrollably but the patient can act controlled and appropriate between these explosive episodes.

5.  Interictal Psychosis (from seizure activity)

Genetic, traumatic, congenital or anoxic lesions or anomalies in the brain that have a low threshold for biochemical changes in the body.  The erratic and excessive neural activity causes spasms in the brain that correspond to dysfunction of the behaviors identified with the affected brain areas.  Not all seizure activity in the brain involves the motor cortex in what is commonly called a convulsion.  Seizure activity in affective and cognitive brain areas modify only the activities governed by the respective area(s) and may have not motor correlates.  Seizure activity in these low threshold brain areas may be triggered by: high fevers, local or systemic infections, hormone fluctuations, fatigue and emotional stress, hyperventilation, hypoxia, ingestion of excessive amounts of water, alcohol, antihistamines, sedatives, or soporifics, hypoglycemia, CVA, trauma, toxins and other more individualized conditions.

Disease/Condition

Pathology

Psychological Changes

a.  Temporal lobe seizures (Psychomotor)

Especially when they occur in the non-dominant side, in the ventro-medial areas of the lobe which connects to the limbic and mid-brain where the emotive brain areas lie.

These result in disturbances in interpretation of the environment and alter affect and cognitive processes between the seizure activity; personalities tend to be hysterical, obsessive-compulsive, and paranoid schizophrenic.

b.  Mixed sensory and temporal lobe seizures

These seizures begin in the sensory cortex and spread to the temporal areas.

Disturbances in sensorium with formed images of visceral, visual, olfactory hallucinations overlaying the typical activity of temporal lobe seizures.

c.  Mixed akinetic and myoclonic seizures and temporal lobe areas

Involvement of the specific areas may not follow any pattern.

Momentary loss of muscle tone or attention, arresting speech or movement overlaying temporal lobe seizure behavior.

d.  Parietal lobe seizures, esp. the left lobe

See Left Parietal Lobe Syndrome

6.  Encephalopathy, Chronic

Secondary changes in cerebral neurons can occur in systemic diseases or in exposure to exogenous toxins.  The pathological changes can be reversed in many instances if the causative agent is discovered and removed before brain damage becomes permanent.  Encephalopathy is associated with neural damage and hemorrhage, producing a variety of neurological symptoms.

Disease/Condition

Pathology

Psychological Changes

a.  Metabolic encephalopathy

     1)  Acidosis

     2)  Uremia

     3)  Azotemia

     4)  Hypoglycemia

     5)  Hypertensive Crisis

     6)  Carbon dioxide

           retention

     7)  Chronic obstructive

           lung disease

     8)  Hyponatremia

Involves many agents.  The most common produces alterations in the internal environment of the body and destroys the homeostasis necessary for cerebral function.  EEG’s are diffusely abnormal with high amplitude delta waves.

In early stages of these metabolic disturbances, there is drowsiness that may progress to stupor.  Mental functions are dulled and the attention span is shortened.  Delerium deepens causing delusions, hallucinations and distortions of perception.  See Fanconi syndrome.

b.  Exogenous encephalopathy

1)  Chronic poisoning

Acute poisoning is usually fatal and exhibits dramatic signs and symptoms other than psychological changes.  It is not considered here although many who are poisoned experience mental changes as part of their symptoms.  This list will enumerate the kinds of poisonings that cause insidious changes in psychological processes and are often mistaken for emotional problems of psychosocial origins.  There are wide individual variations in the extent of the problems manifested by the toxicity of these agents.

Disease/Condition

Pathology

Psychological Changes

a)  Insecticides esp. chloradane rotemone, DDT, PPB

Pathological changes in neural tissue and other organs.

Alters affect and produces depression.

b)  Gaseous poisons, usually industrial; hydrogen sulfide, nitric oxide, nitrogen dioxide, chlorine, ammonia, nickel, phosphorus

Irritate the respiratory tract and decrease the amount of oxygen transferred, producing chronic hypoxia.  Liver and kidneys may be affected and metabolic disturbances occur.

See Metabolic encephalopathy, Renal dysfunction, Hepatic dysfunction.

c)  Carbon monoxide from auto exhaust, cigarette smoke, heating unit ventilation leaks

Binds to hemoglobin and makes it unavailable to body cells; eventual degeneration of basal ganglia.

Headache and irritability, anxious; progresses to visual hallucinations.

d)  Metals

      1 – arsenic, antimony

Segmental demyelination of sensory and motor neurons.

Mental changes and personality disorders.

      2 – mercury, bismuth

Renal insufficiency and malabsorption.  See Malabsorption, Renal dysfunction.

Schizophrenic behavior.

      3 – lead

Myelin degeneration in central nervous system and in peripheral nerves; bone marrow destruction.

See Anemia, Arsenic

      4 – nickel

Damage to lung tissue.

See Gaseous poisons, Anemia

      5 – iron

See Metabolic disorders

      6 – cadmium

            beryllium

Pneumonitis and pulmonary fibrosis.

See Gaseous poisons, Anemia

      7 – thallium

Storage in bone, muscles and brain.

Mental changes and personality disorders.

      8 – manganese,

            magnesium

Degenerative changes in basal ganglia.

See Parkinson Syndrome

      9 – Sodium chloride

            (salt)

Subarachnoid and intraventricular hemorrhage due to capillary rupture, with micro-infarcts in cerebral white matter.

Symptoms depend upon area and extent of damage from the infarct.

e)  Non-metals esp. phosphorus

See Hepatitis, chemical

f)  Volatile organic compounds (esp. ethyl alcohol, ethylene glycol and cyanides)

Fatty changes in the liver, heart and kidneys; fat emboli occasionally to brain with infarcts; loss of neurons from degeneration of myelin sheath, causing moderate to severe cerebral and cerebellar damage.

See Cerebral edema, CVA, Cerebral Lesions, Seizures, Liver dysfunction, Kidney dysfunction.

      1 – carbon tetrachloride

Cirrhosis of the liver and kidney damage.

See Liver dysfunction, Kidney dysfunction.

g)  Volatile aromatic compounds esp. benzene

Anemia; hemorrhage; fatty changes in heart, liver and kidneys.

See Korsafoff’s Syndrome

      1 – camphor

Depresses the central nervous system.

Syndrome resembles acute alcohol poisoning with seizures.

      2 – “glue sniffing”

See Korsakoff’s Syndrome

h)  Salicylates (aspirin)

Affects the brain stem producing hyperventilation with consequent respiratory alkalosis and compensatory metabolic acidosis and ketosis resembling diabetic reaction; blood clotting prothrombin is inhibited, causing bleeding in the micro-circulation of the brain.

Anorexia; renal damage; depression; See kidney dysfunction.

i)  Halogens esp. bromine

Replaces chlorine in the body.

Mental changes with central nervous system depression and stupor, progressing to delusions, hallucinations and mania.

      1 – fluorine

Replaces calcium in the body.

See Hypoglycemia.

7.  Toxic Psychosis

The interruption of neural transmission and/or cerebral function from the accumulation of high levels of abnormal secretions due to a pathological condition, abused drugs, or other therapeutic agents.

Disease/Condition

Pathology

Psychological Changes

a.  Carcinoid Syndrome

Some malignant tumors secrete an excess of serotonin, prostaglandins and other vasoeffective products; sometimes produce a Cushing-like syndrome.

Restricted blood flow to brain.

b.  Therapeutic drug intoxification or side-reaction, esp. reserpine, alpha-methyldopa

Antihypertensive medication which decreases levels of brain catecholamine.

Depression

      1 – non-steroid anti-inflammatory agents e.g. motrin, butazolidin

Alter neural function.

Psychotic symptoms with depression; emotional instability and hallucinations.

c.  Drug abuse intoxication esp. sedatives, narcotics, barbiturates, amphetamines, LSD and other hallucinogens

Excite or depress the central nervous system, often with long term neural dysfunction as sequelae to long term use.

Euphoria; delusions and hallucinations; paranoia; mania; depending upon the drug or drugs used.

8.  Hypervitaminosis

Caused by excessive therapeutic or supplemental doses.

Disease/Condition

Pathology

Psychological Changes

a.  Vitamin A

Defect in body’s storage of carotene or excessive use of therapeutic supplements.

Mimics symptoms of brain tumor with schizophrenic thought and behavior patterms.  See Pseudotumor cerebri.

b.  Vitamin D

Causes elevated levels of calcium.

See Hypercalcemia.

c.  Vitamin K

Associated with hemolytic anemia.

See Anemia.

9.  Cerebral Edema

Swelling of the brain, which interrupts blood flow throughout and causes temporary or permanent damage depending upon the severity of the edema and the amount of time it remains disruptive.  Diminished or absent blood flow results in tissue dysfunction and death.  This condition can be caused by water intoxication, obstructed flow of cerebral spinal fluid, trauma, allergies, encephalopathy and other pathological conditions.  Cerebral function is interrupted bringing alterations in perception, confusion and psychosis.

Disease/Condition

Pathology

Psychological Changes

a.  Pseudotumor cerebri

Edema of the brain caused by Addison’s Disease, Vitamin A hypervitaminosis, Cushing’s Syndrome most often occurs in overweight adolescent or young females who also have menstrual irregularities.

Mimics brain tumors with increased intercranial pressure and psychotic symptoms.

b.  “Pump psychosis”

Cerebral edema that occurs after open heart surgery in some patients who have been on a heart-lung machine.

Confusion, hallucinations, altered perceptions, combative and paranoid – usually temporary.

Endocrine System

Inherited or acquired disorders (often due to a tumor on or in the area of an endocrine gland) of the body’s interconnected endocrine system with hypo- or hyper-secretion of the hormones required for body processes and, therefore, for cerebral activity.

1.  Pituitary

The master gland of the endocrine system, which regulates the hormone production of other endocrine glands.

Disease/Condition

Pathology

Psychological Changes

a.  Hypopituitarism,

     1)  anterior

Congenital or acquired; reduced production of releasing factors which control secretions of other endocrine glands.

See Adrenals, Thyroid, Parathyroid, Gonads.

      2)  posterior (Diabetes

            Insipidus)

Diminished secretion of the antidiuretic hormone, vasopressin, causing increased water loss and dehydration; may be due to pituitary tumor causing compression of the hypothalamus or from injury, emotional shock or infection.

Water loss causes sodium concentration that damages cell walls of cortical neurons and alters their permeability or conduction patterns; vasopressin important in learning process and short term memory.  General confusion, faulty perception; forgetfulness.

      3)  Simmond’s Disease

           (Pituitary cachexia)

A rare hormonal dysfunction with pituitary lesions or destruction of the pituitary from the infection or injury.

Progresses initially from anorexia to premature senility; usually responds with replacement of the missing hormones that depend on pituitary function.

b.  Hyperpituitarism

      1)  anterior

Overstimulation of the endocrine system because of excessive secretion of releasing factors.

See Adrenals, Thyroid, Parathyroid, Gonads.

      2)  posterior

Excessive secretion of vasopressin with water intoxication.

See Cerebral edema, Hydrocephalus.

2.  Thyroid

Primary regulator of body’s metabolic processes, it also plays a role in body growth.

Disease/Condition

Pathology

Psychological Changes

a.  Hypothyroidism (Congenital Cretinism; acquired Myxedema or Hashimoto Disease)

Varies from dysfunction of thyroid secretions to cessation; in adults, this may be due to an autoimmune process or to diminished pituitary secretion.

Metabolism of cerebral neurons slows with loss of metabolites needed for cellular operations; dullness, depression, withdrawal; personality changes.

      1)  Hyperthyroidism

           (Graves Disease)

Excessive secretions of thyroxin with increased cellular metabolism and stimulation of body organs.  May cause hypercalcemia and hypoglycemia.

Increased cerebral activity, with extreme nervousness and tendencies for anxiety complex, extreme worry and paranoia.

3.  Adrenal Glands

Actually, each gland has two independently functioning parts.  The cortex is under the control of pituitary releasing factors, while the medulla is controlled primarily by the sympathetic nervous system.

a.  Medulla

Secretes epinephrine and norepinephrine, which mimic the activities of the sympathetic nervous system with more prolonged response to stress.

Disease/Condition

Pathology

Psychological Changes

      1)  Hyperadrenalism

           (Pheochromacytoma)

An adrenalin-like tumor, located on adrenals or in the pelvic area causing increased secretions of catecholamines; these increase the metabolic rate; may be malignant.

Catecholamines stimulate cerebral activity, dilate pupils; cause perceptual alterations and paranoia; flight-or-fight response; See Hypertension.

b.  Cortex

Secretes mineralcorticoids that help the kidneys regulate the body’s electrolyte balance and secretes glucocorticoids that help regulate the metabolism of carbohydrates, fats and proteins.

Disease/Condition

Pathology

Psychological Changes

     1)  Hypo-

           adrenalcorticoidism

           (Adrenal cortical

           insufficiency or

           Addison’s Disease)

Decreased secretions of aldosterone with excessive sodium loss and electrolyte imbalances; decreased secretion of cortisol with drops in serum glucose; may be caused by tumors, infections, autoimmune diseases or decreased pituitary function.

General depression of body functions, with severe psychological depression, perceptual alterations and paranoia.  See Hypoglycecmia, Cerebrovascular insufficiency.

     2)  Hyper-

           adrenalcorticoidism

           (Cushing’s

           Syndrome)

Congenital or acquired increase in secretions of cortisol, increased serum glucose and decreased protein synthesis; may be the result of adenoma, adenocarcinoma, overproduction of pituitary adrenocorticotropin hormone.

Emotional lability, sleeplessness, agitated depression and paranoia.  See Diabetes Mellitus for symptoms of adrenal-induced diabetes.

     3)  Hyperaldosteronism

Congenital hyperplasia or acquired; adenomas or adenocarcinomas with increased secretion of mineralcorticoids; sodium increases and potassium depletion.

Depression; See Hypernatremia.

4.  Parathyroid

Regulates calcium utilization.

Disease/Condition

Pathology

Psychological Changes

a.  Hypoparathyroidism

Decreased parathyroid function due to tumors on or near the parathyroid gland with decreases in serum calcium.

See Hypocalcemia.

b.  Hyperparahtyroidism

Increased serum calcium levels, with atony of the digestive tract and impairment of the renal tubules causing malabsorption and renal dysfunction; may be caused by dysfunction of the thyroid or adrenal glands.

See Hypercalcemia, Malabsorption and Kidney dysfunction.  Neuromuscular dysfunction with emotional disturbances, somnolence, confusion, muscle weakness and psychosis.

5.  Gonads

Secrete sex hormones that regulate reproductive activity.

Disease/Condition

Pathology

Psychological Changes

a.  Ovaries

      1)  Estrogen deficiency

            (Menopause)

In some menopausal women and in those who have premature cessation of secretions from ovaries; in the latter it may be the result of pituitary tumor or hypopituitarism.

The so-called involutional melancholia characterized by emotional instability, irritability and depression; may have frank psychosis with paranoid delusions.

      2)  Pre-menstrual

            syndrome (PMS)

In some women, about 8-10 days prior to menstruation, the drop in estrogen and progesterone coincide with changes in the body (e.g., increased retention of sodium and water in body tissues); prolactin levels also rise and the release of this pituitary hormone links the ovulation cycle to the systems of brain catecholamines.

Emotional instability, irritability, headache, anorexia, depression, anxiety.

      3)  Post-partum

            psychosis

In some women, slow recovery and/or prolonged disruption of the body’s hormonal balance with depressed estrogen levels and elevated prolactin levels.  See Pre-menstrual syndrome.

May vary from mild depression to severe psychotic depression.

b.  Testes

      1)  Klinefelter’s

            Syndrome

Genetic hypogonadism due to extra X chromosome(s).

Mental and psychological deficiencies vary with extent of chromosomal abnormalities; may have conversion syndrome; violent or criminal behavior.

6.  Menetrier’s Disease

A chronic form of gastritis associated with benign tumors of several endocrine organs, esp. the Islets of Langerhans, pancreas, parathyroid, pituitary and adrenals; hypoproteinemia.  See Endocrine system, Protein deficiency.

Circulatory System

Inherited, congenital or acquired disorders of the cardiovascular-pulmonary systems which interrupt the circulation of oxygenated blood, blood-borne nutrients and enzymes, and metabolic waste products.  Impeded movements of these materials into and away from the neural processes of the brain disrupt their function.

I.  Cardiovascular insufficiency

A decreased ability of the heart to adequately pump blood to meet body needs and/or decreased efficiency of the arteries and capillaries of the system to carry the necessary volume of blood to meet body needs.

Disease/Condition

Pathology

Psychological Changes

a.  Cardiovascular insufficiency, Organic brain syndrome

      1)  Arteriosclerosis

Hardening of middle layer of arterial wall due to deposits of fibrous material and mineral deposits; causes hypertension.

Increased blood pressure, with increased chances of reduced blood flow to the brain, and cerebrovascular accidents.  See Hypertension.

      2)  Atherosclerosis

Occlusion of arterial circulation by fatty deposits on the inner walls of the arteries.

Decreased perfusion of cerebral tissue with acute and/or chronic manifestations varying from transient and non-psychotic personality changes to irreversible neuron damage and psychosis.

      3)  Sub-clavian Steal

A syndrome which follows atherosclerotic changes in left sub-clavian artery causing it to occlude; the result is a deficiency in posterior cerebral blood flow and neural damage in the gray matter of the temporal and occipital lobes.

See Temporal lobe seizures, Left parietal lobe syndrome.

      4)  Carotid

            insufficiency

May be caused by atherosclerosis or carotid body tumors, causing interruption in volume of cerebral blood flow.

See Atherosclerosis.

b.  Congestive heart failure

Decreasing ability of heart to adequately supply blood flow necessary to meet the extensive oxygen and nutrient needs of the brain.

See Atherosclerosis.

c.  Cardiac arrythmias

Irregularities in the heartbeat that reduce cardiac output and blood flow to the brain.

See Atherosclerosis.

Disease/Condition

Pathology

Psychological Changes

2.  Carotid body tumors

Usually benign; interfere with chemoreceptor activity of the carotid, which regulates respiration and cerebral blood flow; faulty determination of cerebral oxygen needs.

See Atherosclerosis, Hypoxia.

3.  Anemias

Because of faulty pigment metabolism, the blood is unable to absorb and deliver oxygen to body tissues, producing tissue hypoxia; this may be caused by alterations in the size and shape of red blood cells (Sickle Cell), abnormal hemoglobin protein, decreased production of  red cells in bone marrow, excessive destruction of red cells, nutritional deficiencies, defective heme synthesis, hyper-spleenism; some forms are inherited, some acquired.

See Hypoxia.

4.  Hypertension

Blood pressure in the range of 200/120 due to various acquired abnormalities of vasoactive hormones and structural anomalies, including encephalopathies; may cause seizures.

Symptoms may resemble those of brain tumors with personality changes, confusion and paranoia; See Neoplasms.

5.  Hypoxia, chronic

Reduced oxygen to the brain from reduced pulmonary efficiency (e.g. lung disease) with decreased oxygenation of the blood; from anemias and decreased circulation.

Symptoms vary from anxiety and confusion to personality disorders with forgetfulness, faulty perception and paranoia.  See Encephalopathy, chronic.

Immune System

Inherited or acquired defects in antigen-antibody processes that may form antibodies directed against the body’s tissues (autoimmune diseases).  These disorders may affect the brain directly, (See cerebral atrophy/sclerosis) or other organs and glands vital to brain metabolism and functioning.

Disease/Condition

Pathology

Psychological Changes

1.  Allergies

Familial; immune response to foreign substances which causes damage through inflammation and swelling; some allergies appear to affect the brain and produce cerebral allergies; in order of prevelance: wheat, beef, milk, sugar and tobacco smoke can cause psychological changes in some people.

In susceptible individuals, euphoria, a feeling of being “out of it,” anger for no particular reason, a sense of being detached from body, nervousness, severe depression, severe mental “blankness.”

2.  Systemic lupus erythmatosis (SLE)

A collagen disease which causes deterioration of connective tissue, esp. soft internal organs, bones and muscles; symptoms may go into remission and exacerbate episodically.

Seizure disorders; schizophrenias; psychosis may be initial feature because of cerebral vasculitis.

3.  Sarcoidosis

Cause unknown; esp. affects blacks, 20-40 years old; tissue destruction of any organ with fibrosis; progresses slowly and may go undetected for several years unless liver, lungs or eyes are affected early.

Any type of central nervous system involvement; the most common are: meningitis, palsey, diabetes insipidus and hypercalcemia.

4.  Multiple sclerosis

Numerous areas of demyelination of nerve fibers throughout the white and gray matter of brain and spinal cord.

Lesions in hippocampus and bilateral limbic structures affect behavior; they may cause severe forms of mania and depression but usually cause euphoria, apathy, lack of judgment, inattention; sudden weeping or laughing with pseudobulbar palsey involving the pathway of emotional control.

5.  Parkinsonism

Degenerative changes in the basal ganglia with depression of the dopamine system.

Depression, to varying degrees.

Malnutrition

Inherited or acquired disorders involving decreased food intake, inadequate breakdown of food from absent or decreased digestive secretions, incomplete- or non-absorption of nutrients from the gastro-intestinal tract, and/or metabolic dysfuction which prevents body utilization of ingested nutrients.

Metabolic Disorders

Chronic disorders in physical and chemical processes and reactions that formulate the ions, atoms and molecules concerned with the disposition of nutrients absorbed into the bloodstream from digestion.

1.  Amino acids

Disease/Condition

Pathology

Psychological Changes

a.  Cystinosis

Genetic; metabolic disturbance with the amino acid cystine which is improperly deposited in the reticuloendothelial system and organs, esp. the kidneys; causes renal insufficiency, uremia and aminoaciduria.

See Fanconi syndrome, Metabolic encephalopathy, Cogan’s syndrome.

b.  Hydroproteinuria

A defect in protein synthesis due to excess of hydropraline oxidase, with amino acid excretion in urine and deficiencies of various kinds of protein molecules.

Emotional instability; See Hypoglycemia, Protein deficiency.

c.  Hypermethianinemia

A defect in protein synthesis with elevation of methianine which is toxic to the central nervous system; in adults, the condition may be subclinical and borderline.

Progressive CNS disturbances with somnolence, hypoglycemia, mental and personality changes; in infants, mental retardation is permanent.

d.  Phenylketonuria

Congenital defect in phenylalamine metabolism with accumulation of high levels in the blood preventing normal brain development.

Mental retardation of varying degrees; schizophrenic symptoms; seizures.

2.  Glucose

Disease/Condition

Pathology

Psychological Changes

a.  von Gierke’s Disease

Abnormal storage of glycogen in the liver; hypoglycemia results; also an inability to participate in the epinephrine stress response with glucose metabolization; may be the result of deficient enzyme; can cause Fanconi-Cogan syndrome.

May be asymptomatic except for chronic hypoglycemia, liver enlargement, anorexia; may lead to seizures; See Hypoglycemia, Fanconi-Cogan syndrome, Seizures.

b.  Forbe’s (Cori) Disease

A glycogen storage disease from a deficiency of the enzyme amyl-1,6-glucosidase with liver enlargement; less severe than von Gierke’s.

See von Gierke’s Disease.

c.  Galactosemia

A genetic or acquired absence of an enzyme in the liver that converts galactose to glucose; intestinal hydrolysis of milk products produces galactose from lactose and its accumulation in the body affects the liver and spleen.

Mental retardation in infants; in older individuals there may be severe personality changes and behavioral disorders that may be psychotic in nature.

3.  Lipids

Disease/Condition

Pathology

Psychological Changes

a.  Hand-Schüller-Christian Disease

A lipid storage disease with abnormal cholesterol and esters deposited in phagocytic cells, esp. in the bones of the face and skull; occurs in young adults.

Involvement of the sella turcia, the bone that lodges against the pituitary and affects the secretions of that gland.  See hypopituitarism.

b.  Amaroutic familial idiocy

See Cerebral atrophy/sclerosis

c.  Schilder’s Disease

A lipid storage disease with progressive sub-cortical encephalopathy.  See Cerebral atrophy/sclerosis-Schilder’s Disease.

4.  Calcium

Disease/Condition

Pathology

Psychological Changes

a.  Hypocalcemia

From decreased parathyroid function or malabsorption syndromes of the GI tract, along with decreased ingestion of fats and Vitamin D; also can be the result of severe alkalosis as in hyperventilation; increased excitability of muscles and neurons; depression of normal heart action and blood coagulation.

Neuromuscular excitability with peychoneurotic, hysterical psychotic manifestations.

b.  Hypercalcemia

From tumors of parathyroid or hyperplasia; may be secondary to renal failure; elevated calcium in turn affects kidneys, lungs and stomach from deposits in these organs.

See Fanconi-cogan Syndrome, Cardiovascular, Hypoxia.

c.  Paget’s Disease (Ostetitis deformans)

Sometimes familial; general thickening and enlargement of bones; when the skull in involved, there is compression of the brain and cranial nerves.

Personality changes dependent upon the size and location of the site of compression; not all patients with this disease experience psychological changes.

5.  Sodium

Disease/Condition

Pathology

Psychological Changes

a.  Hyponatremia, chronic

From infections, tumors, fevers, Diabetes Milletus, chronic renal disease, with water intoxication; low sodium may cause seizures; hypoaldosteronism.

Low sodium causes changes in intracellular-extracellular electrolyte balance that can depress cerebral activity and lead to confusion and eventually to coma.

b.  Hypernatremia, chronic

Elevated serum sodium levels from chronic renal disease, diabetes insipidus, CNS lesions, hyperaldosteronism; produces hypocalcemia.

Decreased calcium affects the permeability of neural cell walls and interferes with sodium-potassium transport; disturbs the electrolyte balance between intracellular and extracellular spaces; causes depression.

6.  Iron (Hemachromatosis or Bronze Disease)

Genetic; iron storage disease caused by hyperabsorptionfrom duodenal mucosa and abnormal deposits in connective tissues, lungs, liver, adrenals, Islets of Langerhans, thyroid and myocardium.

See Hypothyroidism, Diabetes Mellitus, Cirrhosis of liver, Adrenals; signs and symptoms of the disease are secondary to primary damage to body organs.

7.  Porphyria (Hermatoporphyins)

Inherited absence of an enzyme needed to break down the heme in red blood cells leaving iron-free pigments to accumulate.  Some forms are acquired after prolonged alcohol abuse, exposure to toxic chemicals or other conditions that damage the liver.

Often, the first symptoms are neurological with nonspecific degeneration of brain and spinal cord neurons.  Damage is permanent after years of exposure to elevated porphyrins.  Overproduction of porphyrins may be episodic with psychological changes exacerbating and then stabilizing when the excess porphyrins have been excreted.  60% of those affected are catatonic and experience hallucinations; mild psychological changes to frank psychosis.  Many report double vision, frequent abdominal pain, frequent urination and peripheral nerve palsies.  Acute psychotic episodes may be triggered by the use of alcohol and barbiturates.

8.  Copper (Wilson’s Disease)

Genetic; toxic copper deposits in many organs, esp. the liver and the brain; onset adolescence to 40 years of age.

Neurotic to psychotic behavior changes from central nervous system involvement, complicated by liver and kidney dysfunction; usual symptoms of affective schizophrenia.

9.  Hyperthermia

Can be caused by fevers from infections, excessive catabolic processes and exotoxins; alters metabolic processes and rate of metabolism, with changes in cerebral neurons and their susceptibility to high temperatures; may cause permanent damage and produce widespread cerebral dysfunction, esp. of the core areas of brain stem and limbic.

A wide variety of sequelae to prolonged high fevers (greater than 105 degrees in adults is fatal to neurons), range from learning disabilities to psychosis; seizures from lesions; acute phase with delerium and paranoia.

10.  Monoamine oxidase

Levels of serum concentration are inherited; primary responsibility for the degradation of biologic amines and regulation of neurotransmitter concentration.

Reduced levels are associated with auditory hallucinations; it occurs primarily in patients with alcoholism, schizophrenias and manic-depression; elevated levels associated with depressive disorders.

11.  De Sanctis-Cacchione Syndrome

Genetic; from zeroderma pigmentosum, a hypersensitivity to ultraviolet radiation, which causes metabolic changes in DNA, esp. of the skin.  But in this syndrome, there is also neurological involvement.

Signs and symptoms of neural involvement similar to Huntington’s Disease.

12.  Familial hemorrhagic telangiectasia

Genetic; usually not manifested until adulthood; affects the development of blood vessels with deficiencies in the structure of the muscular and connective tissue of the vessels; dilation and sometimes arteriovenous aneurysms with rupture in the microcirculation and multiple mini-hemorrhages causing progressive loss of cerebral functioning; biochemical abnormalities suspected.

See Hemorrhagic lesions.

13.  Ataxia telangiectasia

Familial; telangiectic lesions in the cerebellum causing ataxia and affecting the cerebral cortical pathways which originate near the cerebellum and make contact with it; caused by biochemical abnormality in the IgA and IgG immune system.

Disruptions in the dopaminergic system with motor ataxia and depression.

14.  Lesch-Nyhan Syndrome

An inherited, progressive disorder with overproduction of uric acid.  There is biochemical evidence that uric acid precipitates and interferes with the activity of the neurotransmitters of both central and peripheral nervous systems.  Post-mortems do not show any structural abnormalities.

Mental retardation, spacticity, athetosis and compulsive self-mutilation, disordered perception and thought patterns.

Malabsorption

Reduction or absence of digestive enzymes so that food is not physically and/or chemically prepared for absorption, defects in the intestinal mucosa of those portions of the small intestine that absorb specific molecules, or defects in the selective absorption into the blood stream caused by abnormalities in the composition of blood serum, i.e., enzyme defects, absence of carrier molecules, etc.

Disease/Condition

Pathology

Psychological Changes

1.  Hartnup’s Disease (Heriditary pellagra)

Genetic; malabsorption of tryptophan with decreased conversion of this amine to serotonin.

Cerebellar ataxia and psychosis, with depressive and schizophrenic symptoms.

2.  Hypomagnesuimemia

From decreased absorption in the gut or decreased renal conservation; also from hypothyroidism.

Confusion, delerium, choreiform and athetoid movements, convulsions and paranoia.

3.  Whipple’s Disease (Intestinal lipodystrophy)

Affects males, 30-60 years of age, primarily; may be a virally or bacterially induced defect in reticuloendothelial cells with mechanical lymphocytic blockage of many organs; in GI tract it causes almost total loss of absorbed lipids and thus extremely low levels of cholesterol and triglycerides in the blood.

Results in systemic deficiencies of most nutrients; see esp., the signs and symptoms of vitamin and mineral deficiencies.  See Avitaminosis.

4.  Excessive bacterial flora

Congenital or acquired pocket or loop in the gut with overproduction of bacteria that interferes with absorption by competing for nutrients.

See Avitaminosis.

5.  Disaccharide intolerance (Esp. lactose intolerance; occurs in 20% of Caucasians and 80% of non-white population)

Inherited or acquired destruction of small intestine lining with diarrhea and malnutrition; condition clears up when disaccharides are removed from the diet.

See Avitaminosis.

6.  Celiac Disease

Disease/Condition

Pathology

Psychological Changes

a.  enteropathy

Genetic intolerance to gluten, with changes in the mucosa of the small intestine from rye and wheat protein; decreased absorption produces secondary vitamin deficiencies.

See Avitaminosis.

b.  Exudative enteropathy

Loss of serum protein from mucosa of the GI tract as a result of abnormally permeable lymphatic vessels; decreased serum vitamin levels result from inability of the mucosa to absorb because a protein exudates covers the lumen of the gut.

See Avitaminosis, Hydroproteinuria, Protein deficiency.

c.  Cystic fibrosis

Genetic; manifested usually in infancy and childhood but may not appear until adolescence and young adulthood; the digestive tract is affected, with decreased absorption from the deposits of viscous or solid eosinophilic material which blocks secretions from digestive glands; also abnormal in sodium concentrations in the sweat, parotid and salivary glands; may cause pancreatic insufficiency with signs and symptoms of pancreatitis.

See Avitaminosis, Disaccahride intolerance, Pancreatitis.

d.  Sprue (Idiopathic steatorrhea)

Inherited or acquired (may be the result of tropical infection(s)), hydrolysis of some proteins, which impairs the intestinal mucosa and results in malabsorption esp. of tryptophan, B-12, folic acid; may be gluten intolerance in some cases.

See Avitaminosis, esp. B-12 and folic acid.

7.  Zollinger-Ellison Disease

Non-insulin producing cells of an Islets of Langerhans’ tumor which produces increased gastic secretions and severe peptic ulcer disease; this causes steatorrhea and hemorrhage; 1/3 of the cases also have tumors of the pituitary, parathyroid and adrenals; tumors may be malignant.

See Protein deficiency, Avitaminosis.

Protein deficiency

From inadequate intake, hereditary or acquired anomalies in digestion and absorption of amino acids, in synthesis of proteins from amino acids because of liver disease or the absence of cellular components which carry out protein replication; from accelerated metabolic rate (catabolism), from increased thyroid activity or other body conditions that increase requirements for protein or abnormal loss from the gastrointestinal tract.

Disease/Condition

Pathology

Psychological Changes

1.  Amino acid synthesis defect

Proteins are the substrate for body enzymes which govern all metabolic processes and for the body’s immune system; in the blood, protein provides the basis for the heme molecule’s oxygen transport and for the molecules that maintain serum osmolality, stopping fluid escape from the vascular system and preventing edema.

Cerebral activity diminishes with loss of enzymes needed for neural activity and for the utilization of other nutrients, esp. the B-vitamins; amino acids tyrosine and tryptophan provide the basis for the biogenic amines which are among the brains most important neurotransmitters. See Avitaminosis, Amino acid metabolic defects.

Avitaminosis

From decreased intake of vitamins and/or decreased digestion from malabsorption syndromes and metabolic disorders.   Specific deficiencies affect an individual’s psychological states directly in their absence or insufficient participation in metabolic processes.  Indirectly, vitamin deficiencies may exacerbate other cerebral neuron dysfunctions and syndromes.

1.  Vitamins, acquired or inherited deficiency-related etiological factors.

Disease/Condition

Pathology

Psychological Changes

a.  Wierneke’s encephalopathy

Deficiency in thiamine (B-1) that interrupts the glucose pathway and carbohydrate metabolism leading to depression of glucose supply to meet the brain’s extensive needs for glucose.

Chronic deficiency causes brain lesions; “cerebral beriberi,” a condition of acute hemorrhagic encephalopathy with decreased blood flow into some areas; mental confusion, palsey and ataxia.  Contributes to the neural destruction in Korsakoff’s syndrome; insomnia, nervousness, irritability, confusion, depression, hallucinations.

b.  Riboflavin

Deficiency in vitamin B-2 affects the pyrodoxine pathway contributin to pyrodoxine deficiency anemia which interrupts cellular utilization of oxygen.

See Pyrodoxine hydrochloride; causes depression.

c.  Niacin

Deficiency in vitamin B-3 interrupts tryptophan and carbohydrate metabolism as well as some nucleic acid synthesis, with deterioration of cells of the skin, digestive tract and brain.

The brain shows edema and loss of ganglion cells; the spinal cord undergoes focal demyelination of lateral and posterior columns; administration of niacin removes schizophrenic symptoms in some patients; see Hypoglycemia.

d.  Pyrodoxine hydrochloride

Vitamin B-6 deficiency interrupts the metabolism of amino acid tryptophan and of some fatty acids; can cause undersized red blood cells, microcytic anemia.

Hereditary refactory sideroblastic anemia, caused by a block in the capacity of the blood to carry oxygen; will respond to large doses of B-6; see Anemia; treatment of some autistic children shows decreases in withdrawal behavior.

e.  Cyancobalamine (Vitamin B-12)

Deficiency interrupts DNA synthesis in the bone marrow with production of enlarged and short-lived red blood cells; interrupts DNA synthesis of myelin formation on cerebral and spinal nerves.

Difficulty in learning and memory, euphoria, perceptual alteration, depressive withdrawal, agitation, psychotic behavior with mania, hallucinations and paranoia; causes pernicious anemia; see Anemias.

f.  Folic acid

Deficiency in this B-group nutrient interrupts cell division, DNA-RNA synthesis in the bone marrow contributing to pernicious anemia by inteferring with utilization of Vitamin B-12 and pantothenic acid; interrupts amino acid and glucose utilization.

See Cyancobalamine; Hypoglycemia, withdrawal depression.

g.  Pantothenic acid (Calcium pentothenate, a B-group nutrient)

Deficiency interrupts use of fat and glucose; adrenals become enlarged, hemorrhagic and unable to produce normal amounts of hormones; interrupts the immune response; has an anticholinergic effect on the GI tract, with decreased secretions from the pancreas.

Depression, inability to handle stress; see Hypoglycemia; Adrenal cortical insufficiency; Malabsorption.

h.  Biotin

Deficiency of this B-group nutrient interrupts cellular metabolism.

Depression, panic, halluncinations, suicidal tendencies.

Disease/Condition

Pathology

Psychological Changes

2.  Vitamin C

Deficiency interrupts the reduction of folic acid to a metabolically active form; interrupts the absorption of iron from the GI tract; interrupts synthesis and metabolism of some amino acids, esp. tyrosine, which is the precursor to some neurotransmitters; may serve as an antioxidant, allowing more oxygen to be utilized inside body cells.

Administration provides improvement in some schizophrenias; see Folic acid, Anemias.

3.  Vitamin D

Deficiency interrupts the absorption of calcium from the GI tract, interrupts the metabolism of calcium and Vitamin K.

See Hypocalcemia, Vitamin K.

4.  Vitamin E

Deficiency produces decreased tolerance of red blood cell membrane to damaging effects of oxidants in the blood and reduces their life span; if accompanies protein deficiency, it decreases the production of red blood cells.

See Anemias.

5.  Vitamin K

Deficiency prolongs the clotting time of the blood.

One of the major causes of cerebral hemorrhage; see Cerebral hemorrhage.

Hypoglycemia

Acquired or inherited disorders that affect digestion: malabsorption syndromes of metabolic defects along with inadequate calorie intake are common.  These decreases in the glucose available to the brain cells may precipitate seizures and depress central nervous system activity.

Disease/Condition

Pathology

Psychological Changes

1.  Addison’s Disease

See Adrenal cortical insufficiency.

2.  Hyperinsulinism

Overproduction of insulin due to tumor or hyperplasia of the Islets of Langerhans; causes high serum insulin levels with corresponding drops in serum glucose.

Depression of central nervous system neuron activity with excitation followed quickly by anxiety, confusion, hallucinations and coma; chronic condition produces behavior changes with lassitude and paranoia.

3.  Hypopituitarism, anterior

See Endocrine System, hypopituitarism, Adrenal cortical insufficiency.

4.  Hepatic disease

Damage e.g., sclerosis, prevents mobilization to glucagen to meet low blood sugar needs.

See Hyperinsulinism.

5.  Starvation

See Protein-calorie malnutrition.

See Hyperinsulinism.

6.  Increased catabolism

Cachexia from carcinomatosis and epinephrine producing tumors, such as phenochromacytoma; hyperthyroidism.

See Hyperinsulinism.

Protein-calorie Malnutrition (PCM)

Disease/Condition

Pathology

Psychological Changes

1.  Prenatal, infants, early childhood

In the pre-natal period, PCM decreases the number of neurons that will develop; in the immediate post-natal period, PCM decreases the process of neural myelination and the number of dendrite formations that can form.  Also interrupts the neural development of the cerebellum; in early childhood, up to three or four years of age, it prevents the development of dendrite connections, esp. if there is a concomitant deprivation of sensory stimulation which is often the case with a lethargic and sickly, malnourished child; permanent brain damage.

As the child develops, there is a decreased ability to respond to new situations with adaptive responses; there is diffuse brain dysfunction with learning and behavior problems from the child’s inability to form abstractions and to generalize from his experiences; paranoia.  See Minimal brain dysfunction.

2.  Late childhood and adults

Reduction of glucose, protein and vitamin stores to meet stress, fight infection and interact with environment for learning, development and survival.

Usually temporary psychological changes from disruption of neural metabolism; extensive or chronic deprivation may result in permanent brain damage and alterations in thought and behavior patterns.

Other chronic organ dysfunctions

Inherited, congenital or acquired disorders that inhibit or eliminate the synthesis of enzymatic molecules for cerebral function, the presence of glucose and oxygen for cellular use and the elimination of toxic metabolites from circulating blood.  Failure to perform any of these functions disrupts normal neural activity.

Renal dysfunction

Abnormal kidneys may produce syndromes related to imbalances in the body’s electrolytes and mineral levels, in the loss of serum proteins and glucose and the accumulation of toxic metabolites and water products.  These provide for alterations in the internal environment of the body, which can seriously disrupt the functions of all cells, especially the delicate cerebral neurons.

Disease/Condition

Pathology

Psychological Changes

1.  Fanconi syndrome

Acquired or familial slow progressing kidney disease, with degeneration of the renal parenchyma and metabolic disorders from congenital anomalies in the structure of the kidneys and damage to them from toxic materials deposited in the renal tubules.

See Encephalopathy, metabolic.

2.  Cogan’s syndrome

Adult form of Fanconi syndrome

See Fanconi Syndrome

3.  Uremia

High serum concentrations of nitrogenous waste products accumulate from various sources; infection, trauma, congenital defects or hypertension; all of which cause damage to the kidneys; toxic blood levels of various substances also produces deficiencies in kidney function.

Irritability, tremors, paranoia, convulsions, coma.

Pancreatic dysfunction

Abnormal pancreatic function results in loss of necessary pancreatic enzymes, for digestion and/or abnormal secretion of insulin, either too much or too little to accommodate adequate cellular use of glucose by the body’s cells and especially the cerebral neurons.  The latter have no way to mobilize existing glucose stores and can provide emergency glucose for only a few minutes before brain operations are seriously altered.

Disease/Condition

Pathology

Psychological Changes

1.  Diabetes Mellitus esp. as chronic, sub-clinical and untreated

A disorder of carbohydrate metabolism with loss of ability to oxidize and utilize carbohydrates; results from dysfunction of normal insulin mechanism; familial or acquired through infection, atherosclerosis or thrombosis; may be due to Cushing’s disease from prolonged elevation of serum glucose and over-stimulation of the Islets of Langerhans.

Chronic high blood glucose levels and acidosis cause microscopic changes in capillaries of body organs, including brain, with a thickening of the capillary walls and inhibition of oxygen and nutrients as well as waste product removal; depression, often psychotic.

a.  Hypoinsulinism

See Hypoglycemia.

b.  Pancreatitis, chronic and subclinical

Permanent destruction of acini with digestive enzyme secretions and lesser damage to Islets of Langerhans with insulin dysfunction; may cause diabetes mellitus, malabsorption from loss of enzymes and duodenal ulcer from absence of acid-neutralizing secretions.

See Avitaminosis, Diabetes mellitus, Malabsorption.

Hepatic dysfunction

Abnormal liver function interferes with the synthesis of some body proteins, especially those that function as enzymes, with the degradation of some waste products and drugs to an excretable form, with the secretion of bile for the digestion of fats, with the synthesis of blood clotting factors and with the storage of glucose in the form of glycogen.

Disease/Condition

Pathology

Psychological Changes

1.  Hepatitis, viral (A and B)

Chronic form persists undetected and there are relapses in 5% of the cases, with the only evidence of the disease being increased impairment of functions without clinical evidence of inflammation; parenchymal cells of the liver degenerate.

See Malnutrition, Encephalopathy, metabolic; Hypoglycemia.

2.  Hepatitis, chemical and plasma cell (Lupoid)

See Hepatitis, viral

3.  Cirrhosis

Progressive, degenerative and diffuse inflammation of the liver, especially from chronic alcoholism, with permanent destruction of the parenchymal cells.

See Encephalopathy, metabolic; Hepatitis; Amino acid defect; Cerebral lesions, syndrome; Seizures.