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Neurobehavioral Disorders

(9-10-14)

Terminology

Cognitive, behavioral, and emotional disorders associated with damage or dysfunction in the CNS. In the past these have been labeled as “Organic Mental Syndromes/Disorders” “Organic Brain Syndromes” “OBS”; Strub & Black (1981) prefer “Neurobehavioral Disorders”

DSM 5 uses the terminology: neurocognitive disorders

DSM-IV-TR uses the terminology: COGNITIVE DISORDERS

“Delirium, Dementia, and Amnestic and other Cognitive Disorders”

where the primary difficulty is a disturbance in cognition or memory, and the etiology is assumed to be either a “general medical condition” or a substance (drug of abuse, medication, toxin).

Within the other major groupings of Mental Disorders in DSM-IV there are categories to cover cases where brain damage or disease are believed to be the cause of the problems, e.g., “Conditionor Personality Change associated with a General Medical Condition.”

Anatomy of Behavior

  1. Ascending reticular systems (brain stem)
    • arousal/(editing)
  2. Limbic systems (subcortical)
    • arousal/attention/(editing)
    • biological drives (basic instincts)
    • emotional behavior/reinforcement
    • temperament (?)
    • consolidation of verbal learning/memory
  3. Cortex
    • sensory unit: processing input
      • posterior: temporal, parietal, & occipital lobes
    • motor unit: executive functions, “pause and plan”
      • frontal: frontal lobe
        • arousal/attention/(editing)
        • forming plans
        • executing plans
        • verifying results

Neurobehavioral Disorders

  1. Acute Confusional States (Delirium)
    • alternative terminology: encephalopathy (neurologists may use this term), delirium, altered mental status (ER physicians may use this), acute confusional state
    • Causes of Delirium
    • “A RAPIDLY DEVELOPING, YET FLUCTUATING, REVERSIBLE CHANGE IN BEHAVIOR THAT IS CHARACTERIZED BY A CLOUDING OF CONSCIOUSNESS, INCOHERENCE IN THE TRAIN OF THOUGHT, AND DIFFICULTY WITH ATTENTION AND CONCENTRATION.” (STRUB & BLACK, P. 109).
    • REDUCED CLARITY OF AWARENESS OF ENVIRONMENT
    • DISORIENTATION.
    • CONFUSION
    • INATTENTION
  2. Dementia
  3. Amnestic Syndromes: memory
    • declarative/semantic/verbal
    • procedural/nonverbal (?)
  4. Focal Lesion Syndromes
    • Aphasias: DISTURBANCE CAUSED BY DAMAGE TO LANGUAGE AREAS OF THE BRAIN
      • Broca’s Aphasia expressive
      • Wernicke’s Aphasia receptive
    • Apraxia: “DISORDER IN CARRYING OUT OR LEARNING COMPLEX MOVEMENTS that cannot be accounted for by strength, coordination, sensation, comprehension, or attention.” (p. 274)
      • Ideomotor Apraxia
      • Constructional Apraxia
    • Agnosia: DEFICIT IN OBJECT RECOGNITION IN ABSENCE OF ANY DISTURBANCE IN PRIMARY SENSORY SYSTEM (P. 278)
      • Visual Agnosia
      • Prosopagnosia: INABILITY TO RECOGNIZE FAMILIAR FACES
    • Frontal Lobe Syndromes
      • Disinhibited: POOR JUDGEMENT, UNINHIBITED SOCIAL BEHAVIOR, CRUDE LANGUAGE & HUMOR, IMPULSIVE
      • Amotivational: APATHETIC, LOW ENERGY LEVEL, LACK OF SPONTANEOUS BEHAVIOR
    • Limbic Syndromes
      • Amnesiac Syndrome
      • psuedopsychiatric syndromes
        • “epileptic personality [disorder]”: perseveration, excessive religiosity, paranoia, egocentric selfishness, impulsivity, mental slowness, emotional viscosity, circumstantiality, irritability, mood fluctuations

Etiologies Associated with Neurobehavioral Disorders

  1. Head injuries
    • Donders & Hoffman (2002) found that male gender was associated with an increased risk for retrieval deficits on the CVLT-C after pediatric TBI, possibly due to reduced speed or efficiency of information processing.
    • penetrating brain damage
    • closed head injuries
    • Glasgow Coma Scale
  2. Cerebrovascular disease
    • stroke
    • occlusion
    • hemorrhagic
    • transient ischemic attack (TIA)
    • arterial-venial malformation (AVM)
  3. Tumor
  4. Metabolic disorder
    • Phenylketonia (PKU)
  5. Infection
    • encephalitis
    • Acquired Immune Deficiency Syndrome: AIDS Related Dementia
  6. Toxic exposure
    • heavy metals: lead, mercury
    • organic solvents: sniffing glue
    • alcohol: intoxication, withdrawal (delirium tremens)

References

American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Text Revision. (4th ed.), Washington DC: Author, 2000.

Arciniegas, D.B. & Beresford, T.P. (2001). Neuropsychiatry: An introductory approach. New York: Cambridge University Press.

Kolb, Bryan & Whinshaw, Ian Q. Fundamentals of Human Neuropsychology. (4th ed.), New York: W.H. Freeman and Company, 1995.

Martin, G. Neil. Human Neuropsychology. London: Prentice Hall Europe, 1998.

Moscovitch, M. & Rozin, P. Disorders of the nervous system and psychopathology. Rosenhan, D.L. & Seligman, M.E.P. Abnormal Psychology, 3rd Ed., pp. 645-692. New York: W.W. Norton. 1995.

Sacks, Oliver. The Man Who Mistook His Wife for a Hat and Other Clinical Tales. New York: Harper & Row, 1985.

Strub, Richard L. & Black, F. William. Neurobehavioral Disorders: A Clinical Approach. Philadelphia: F.A. Davis Company, 1981.

Causes of Delirium

(10-20-03)

I WATCH DEATH

I: Infections

W: Withdrawal
A: Acute metabolic disorders
T: Trauma
C: CNS Pathology
H: Hypoxia
D: Deficiencies
E: Endocrinopathies
A: Acute vascular
T: Toxins/Drugs
H: Heavy metals

Subtypes of Dementia

The subtypes that had been available in DSM-IV to qualify all dementias further (With Delirium, With Delusions, With Depressed Mood, Uncomplicated) are now only available for Vascular Dementia:


“By ICD-9-CM convention, Vascular Dementia is the only type of dementia that employs subtypes to indicate the presence of significant associated symptoms.” (p. 158)


“The specifier With Behavioral Disturbance (which cannot be coded) can also be used to indicate significant behavioral disturbances (e.g., wandering).” (p. 159)


Delusions are noted as common associated symptoms of Dementia (p. 150). Psychotic symptoms are noted as associated symptoms of Dementia of the Alzeheimer’s Type (p. 297).

Alzheimer’s disease & genes

* Researchers have reported new findings concerning the increased risk of Alzheimer’s disease among people who inherit mutations in the presenilin genes.

  • note: an estimated 40% of people with familial Alzheimer’s disease have presenilin gene mutations.
  • researchers at Harvard Medical School report that alterations made in the presenilin-1 gene in cultured laboratory cells resulted in the inhibition of beta-amyloid precursor protein and in lower levels of amyloid-beta protein, which forms the brain lesions found in Alzheimer’s patients.
  • authors say the findings suggest that presenilin may be the long-sought enzyme that is responsible for the overproduction of beta-amyloid in Alzheimer’s patients.
  • the findings are in the journal Nature (1999;398:466-467).

DAT & Depression

Zubenko, Zubenko, McPherson, Spoor, Marin, Fawlow, Smith, Geda, Cummings, Petersen, & Sunderland (2003) present data supporting the validity of a specific syndrome:

Major Depressive Syndrome of Alzheimer’s Disease

They feel this is a distinct diagnostic entity and “may be among the most common mood disorders of late life.” (p. 865)

Alzheimer’s Disease, amyloid beta, & tau

both abnormal accumulations of amyloid beta and of tau may result in the cognitive losses of Alzheimer’s dementia.

Current neuroenhancement medications are aimed at reducing production of amyloid beta; these slow decline but only temporarily.

Animal models (mice genetically engineered to develop brain pathology similar to Alzheimer’s disease) suggest that treatment reducing the formation of mutant taus or even the normal protein may reduce memory loss and neurological deficits even with accumulating amyloid beta (see Roberson et al., 2007).

Mutant tau may activate microglial cells, the brain’s immune cells. Treatment with an immunosuppressant decreases neuronal loss and life span in affected mice.

Also, tau binds to and stabilizes the microtubles which transport nutrients, proteins, and material in the neuronal axon. Tau become excessively phosphorylated in Alzheimer’s brains, leading to it no longer binding properly to microtubules, that in turn deteriorate, leading to cell death.

Science, vol 316, 2007, pp. 1416-1417.

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