THE NEUROCOGNITIVE DISORDERS

MELDI A. ANUTA, M.D., FPNA, FPCP

ATENEO DE DAVAO UNIVERSITY
SEPTEMBER 20, 2014
 REFERENCES
•DSM 5
•Kaplan & Sadock’s Synopsis of Psychiatry
9th edition
•Adams & Victor’s Principles of Neurology
9th edition by Ropper & Samuels
•Harrison’s Principles of Internal Medicine
17th edition by Fauci et al
NEUROCOGNITIVE FUNCTIONS
•cognitive functions closely linked to the
function of particular areas, neural
pathways, or cortical networks in the
brain substrate layers of neurological
matrix at the cellular molecular level.
•Neuropsychology & Cognitive
neuroscience
NEUROCOGNITIVE DEFICIT
a reduction or impairment of cognitive
function in any of the areas of
cognition, but particularly when
physical changes can be seen to have
occurred in the brain, such as after
neurological illness, mental illness,
drug use, or brain injury.
NEUROCOGNITIVE DEFICIT
CRITERIA BASED ON DETAILED
COGNITIVE DOMAINS
NEUROCOGNITIVE DOMAINS
•COMPLEX ATTENTION
•EXECUTIVE FUNCTION
•LEARNING & MEMORY
•LANGUAGE
•PERCEPTUAL–MOTOR
•SOCIAL COGNITION
 CLINICAL NEUROPSYCHOLOGIST
One who specializes in using neuropsychological
tests to detect & understand neurocognitive deficits, &
may be involved in the rehabilitation of an affected
person
May adopt non-invasive procedures such as the
(CML) cognitive psychotherapists.
COGNITIVE NEUROPSCYHOLOGY - the discipline
that studies neurocognitive deficits to infer normal
psychological function
Photograph of the lateral surface of the human brain. (Reproduced by permission from Carpenter MB, Sutin J
Cytoarchitectural zones
of the human cerebral
cortex according to
Brodmann. A. Lateral
surface. B. Medial
surface. C. Basal
inferior surface
DERANGEMENTS OF INTELLECT,
BEHAVIOR & LANGUAGE DUE TO
DIFFUSE & FOCAL
NEUROLOGIC DISEASES
DELIRIUM & OTHER ACUTE
CONFUSIONAL STATES
DEMENTIA & ACUTE AMNESIC
(KORSAKOFF) SYNDROME
NEUROLOGIC DISORDERS
CAUSED BY LESIONS IN CERTAIN
PARTS OF THE CEREBRUM
DISORDERS OF SPEECH &
LANGUAGE
 CONFUSION
CONFUSION

a mental & behavioral state of

reduced comprehension,
coherence, & capacity to reason
one of the most common
problems encountered in
medicine
 DELIRIUM
a term used to describe an acute
confusional state
remains a major cause of M & M rates,
costing billions of dollars yearly in health
care costs in the US alone
often goes unrecognized despite clear
evidence that it is usually the cognitive
manifestation of serious underlying medical
or neurologic illness
 TERMS TO DESCRIBE DELIRIUM

Encephalopathy
Acute brain failure
Acute confusional state
Postoperative or ICU psychosis
 DEFINITION

A disturbance in attention &

awareness
a relatively acute decline in
cognition that fluctuates over hours
or days
 DELIRIUM
A disturbance in attention & awareness
Develops over a short period of time ( hours or
days) , represents a change from baseline attention
& awareness, & tends to fluctuate in severity
during the course of a day
An additional disturbance in cognition
Not better explained by another neurocognitive
disorder
Evidence of being a direct consequence of
another medical condition, substance intoxication,
or withdrawal , or exposure to a toxin, or is due to
multiple etiologies
 TYPES
SUBSTANCE INTOXICATION DELIRIUM
SUBSTANCE WITHDRAWAL DELIRIUM
MEDICATION-INDUCED DELIRIUM
DELIRIUM DUE TO ANOTHER MEDICAL
CONDITION
DELIRIUM DUE TO MULTIPLE
ETIOLOGIES
 DELIRIUM
SPECIFY IF
ACUTE (HOURS OR DAYS)
PERSISTENT (WEEKS OR MONTHS)
SPECIFY IF
HYPERACTIVE (mood lability,
agitation, refusal to cooperate)
HYPOACTIVE (sluggishness &
lethargy)
MIXED LEVEL OF ACTIVITY
 DELIRIUM
OTHER SPECIFIED DELIRIUM
Symptoms predominate but do not meet the
full criteria for delirium
Clinician chooses to communicate the specific
reason that the presentation does not meet the
criteria
UNSPECIFIED DELIRIUM
Symptoms predominate but do not meet the
full criteria for delirium
Clinician chooses not to specify the reason
that the criteria are not met
 DELIRIUM
HALLMARK - a deficit of attention, although all
cognitive domains—including memory, executive
function, visuospatial tasks, and language—are
variably involved.
Associated symptoms :
altered sleep-wake cycles
perceptual disturbances (hallucinations or
delusions)
affect changes
autonomic findings
HYPERACTIVE VS HYPOACTIVE
SUBTYPES
SEVERE ALCOHOL WITHDRAWAL
prominent hallucinations, agitation, and
hyperarousal, often accompanied by life-
threatening autonomic instability
OPIATE INTOXICATION
withdrawn and quiet, with prominent
apathy and psychomotor slowing
 DELIRIUM
Reversible
Can be treated easily
Long-term cognitive effects remain
largely unknown & understudied
Some episodes continue for
weeks, months, or even years
 RISK FACTORS
2 most consistently identified risks
older age
baseline cognitive dysfunction
 Individuals who are over age 65
or exhibit low scores on
standardized tests of cognition
develop delirium upon
hospitalization at a rate approaching
50%.
 RISK FACTORS

Other predisposing factors

sensory deprivation
indices for poor overall health
(baseline immobility, malnutrition,
& underlying medical or neurologic
illness)
 IN-HOSPITAL RISKS
use of bladder catheterization
physical restraints
sleep and sensory deprivation
the addition of three or more new
medications
Surgical and anesthetic risk factors
specific procedures such as those
involving cardiopulmonary bypass
inadequate or excessive treatment of
pain in the immediate postoperative period
DELIRIUM & DEMENTIA
MAY OVERLAP.
 EPIDEMIOLOGY
 A common disease
 Hospitalized patients - 14 to 56%, with
higher rates reported for elderly patients
and patients undergoing hip surgery
 Older patients in the ICU have especially
high rates of delirium (70 to 87%)
 Not recognized in up to 1/3 of delirious
inpatients
 EPIDEMIOLOGY
 Diagnosis is especially problematic
in the ICU environment
 Outside the acute hospital setting
- nearly 2/3 of patients in nursing
homes & in over 80% of those at
the end of life
 APPROACH
 DIAGNOSIS IS CLINICAL – HISTORY & P.E.
 SCREENING TOOLS
 Confusion Assessment Method (CAM);
 Organic Brain Syndrome Scale;
 Delirium Rating Scale;
 Delirium Detection Score (in the ICU)
 ICU version of the CAM
 CAM
 1) an acute onset and fluctuating course
 2) inattention accompanied by either
 3) disorganized thinking or
 4) an altered level of consciousness
COMMON ETIOLOGIES
CEREBROVASCULAR DISEASES
BRAIN TUMORS
C.N.S. INFECTIONS
METABOLIC ENCEPHALOPATHIES
TOXINS
SEIZURE-RELATED DISORDERS
ENDOCRINOLOGIC CONDITIONS
AUTOIMMUNE DISORDERS
HOSPITALIZATION
TERMINAL END-OF-LIFE DELIRIUM
 MAJOR & MILD
NEUROCOGNITIVE DISORDERS
MAJOR NEUROCOGNITIVE DISORDER
Evidence of significant cognitive decline from a
previous level of performance one one or more
cognitive domains based on
Concern that there has been a significant
decline in cognitive function
A substantial impairment in cognitive
performance, preferable documented by
standardized neuropsychological testing or,
in its absence, another quantified clinical
assessment
MAJOR NEUROCOGNITIVE DISORDER

The cognitive deficits interfere with

independence in everyday activities.
The cognitive deficits do not occur
exclusively in the context of delirium.
The cognitive deficits are not better
explained by another mental disorder.
SPECIFY WHETHER DUE TO
ALZHEIMER’S DISEASE
FRONTOTEMPORAL LOBAR DEGENERATION
LEWY BODY DISEASE
VASCULAR DISEASE
TRAUMATIC BRAIN INJURY
SUBSTANCE / MEDICATION USE
HIV INFECTION
PRION DISEASE
PARKINSON DISEASE
HUNTINGTON’S DISEASE
ANOTHER MEDICATION CONDITION
MULTIPLE ETIOLOGIES
UNSPECIFIED
 SPECIFY IF

WITHOUT BEHAVIORAL DISTURBANCE

WITH BEHAVIORAL DISTURBANCE

MILD (INSTRUMENTAL ACTIVITIES)

MODERATE (BASIC ACTIVITIES)
SEVERE (FULLY DEPENDENT)
MILD NEUROCOGNITIVE DISEASE
EVIDENCE OF A MODEST COGNITIVE
DECLINE FROM A PREVIOUS LEVEL OF
PERFORMANCE IN ONE OR MORE
COGNITIVE DOMAINS BASED ON
CONCERN THAT THERE HAS BEEN A
MILD DECLINE IN COGNITIVE FUNCTION
A MODEST IMPAIRMENT IN COGNITIVE
PERFORMANCE
MILD NEUROCOGNITIVE DISEASE
THE COGNITIVE DEFICITS DO NOT
INTERFERE WITH CAPACITY FOR
INDEPENDENCE IN EVERYDAY ACTIVITIES
THE COGNITIVE DEFICITS DO NOT OCCUR
EXCLUSIVELY IN THE CONTEXT OF A
DELIRIUM
THE COGNITIVE DEFICITS ARE NOT
BETTER EXPLAINED BY ANOTHER MENTAL
DISORDER
SPECIFY WHETHER DUE TO
ALZHEIMER’S DISEASE
FRONTOTEMPORAL LOBAR DEGENERATION
LEWY BODY DISEASE
VASCULAR DISEASE
TRAUMATIC BRAIN INJURY
SUBSTANCE / MEDICATION USE
HIV INFECTION
PRION DISEASE
PARKINSON DISEASE
HUNTINGTON’S DISEASE
ANOTHER MEDICATION CONDITION
MULTIPLE ETIOLOGIES
UNSPECIFIED
 SPECIFY IF

WITHOUT BEHAVIORAL DISTURBANCE

WITH BEHAVIORAL DISTURBANCE
ALZHEIMER’S DISEASE
 MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO ALZHEIMER’S DISEASE
THE CRITERIA ARE MET FOR MAJOR OR
MILD NEUROCOGNITIVE DISORDER
THERE IS INSIDIOUS ONSET AND
GRADUAL PROGRESSION OF IMPAIRMENT
IN 1 OR MORE COGNITIVE DOMAINS (AT
LEAST 2 IF MAJOR)
CRITERIA ARE MET FOR EITHER
PROBABLE OR POSSIBLE ALZHEIMER’S
DISEASE (A.D.)
MAJOR NEUROCOGNITIVE DISORDER

PROBABLE A.D. IS DIAGNOSED IF

EITHER OF THE FOLLOWING IS
PRESENT, OTHERWISE POSSIBLE
A.D. SHOULD BE DIAGNOSED
EVIDENCE OF A CAUSATIVE A.D.
GENETIC MUTATION
ALL 3 FEATURES ARE PRESENT
MAJOR NEUROCOGNITIVE DISORDER

PROBABLE A.D. IS DIAGNOSED IF

EITHER OF THE FOLLOWING IS
PRESENT, OTHERWISE POSSIBLE
A.D. SHOULD BE DIAGNOSED
EVIDENCE OF A CAUSATIVE A.D.
GENETIC MUTATION
ALL 3 FEATURES ARE PRESENT
 MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO ALZHEIMER’S DISEASE
3 FEATURES
CLEAR EVIDENCE OF DECLINE IN
MEMORY & LEARNING & AT LEAST 1
OTHER COGNITIVE DOMAIN (BASED ON
DETAILED HISTORY OR SERIAL N.P.
TESTING
STEADILY PROGRESSIVE, GRADUAL
DECLINE IN COGNITION, WITHOUT
EXTENDED PLATEAUS
NO EVIDENCE OF MIXED ETIOLOGY
MILD NEUROCOGNITIVE DISORDER

PROBABLE A.D. IS DIAGNOSED IF

THERE IS EVIDENCE OF A
CAUSATIVE A.D. GENETIC
MUTATION FROM EITHER GENETIC
TESTING OR FAMILY HISTORY
 MILD NEUROCOGNITIVE DISORDER
POSSIBLE A.D. IS DIAGNOSED IF THERE IS
NO EVIDENCE OF A CAUSATIVE A.D. GENETIC
MUTATION FROM EITHER GENETIC TESTING
OR FAMILY HISTORY & ALL 3 OF THE
FOLLOWING ARE PRESENT :
CLEAR EVIDENCE OF DECLINE IN
MEMORY & LEARNING
STEADILY PROGRESSIVE, GRADUAL
DECLINE IN COGNITION, WITHOUT
EXTENDED PLATEAUS
NO EVIDENCE OF MIXED ETIOLOGY
MILD NEUROCOGNITIVE DISORDER

THE DISTURBANCE IS NOT BETTER

EXPLAINED BY
CEREBROVASCULAR DISEASE,
 ANOTHER NEURODEGENERATIVE
DISEASE,
THE EFFECTS OF A SUBSTANCE, OR
ANOTHER MENTAL, NEUROLOGICAL,
OR SYSTEMIC DISORDER
 DEGENERATIVE BRAIN BRAIN TUMOR
DISEASE
CHRONIC SUBDURAL
MULTIPLE STROKES HEMATOMA

CHRONIC
CHRONIC DRUG MENINGOENCEPHALITIS
INTOXICATION

NORMAL-PRESSURE DEPRESSIVE ILLNESS

HYDROCEPHALUS

ETIOLOGIES
 ALZHEIMER’S DISEASE

 2O MILLION PEOPLE WITH DEMENTIA

WORLDWIDE
 66% IN DEVELOPING COUNTRIES
 ONLY 3.2% OF MILD CASES DIAGNOSED.
 ONLY 24% OF MODERATE TO SEVERE
CASES DETECTED.
CELL DYSFUNCTION & DEATH IN NUCLEAR GROUPS OF NEURONS
RESPONSIBLE FOR MAINTENANCE OF SPECIFIC TRANSMITTER SYSTEMS LEAD
TO DEFICITS IN ACETYLCHOLINE, NOREPINEPHRINE & SEROTONIN.
MAJOR OR MILD FRONTOTEMPORAL
NEUROCOGNITIVE DISORDER
MAJOR OR MILD FRONTOTEMPORAL
NEUROCOGNITIVE DISORDER
•Often begins in the fifth to seventh decades
•Nearly as prevalent as AD
•Behavioral symptoms predominate in the
early stages of FTD
•Autosomal dominant inheritance is seen in
about 10%
•The most common autosomal dominantly
inherited mutations causing FTD involve the
MAPT or GRN genes
MAJOR OR MILD FRONTOTEMPORAL
NEUROCOGNITIVE DISORDER
•The distinguishing anatomic hallmark of
FTD is a focal atrophy of frontal, insular,
and/or temporal cortex.
•Microscopic findings seen across all
patients with FTD include gliosis,
microvacuolation, and neuronal loss.
MAJOR OR MILD NEUROCOGNITIVE
DISORDER WITH LEWY BODIES
 MAJOR OR MILD NEUROCOGNITIVE
DISORDER WITH LEWY BODIES
•The presence of Lewy bodies and Lewy neurites
throughout specific brainstem nuclei, substantia
nigra, amygdala, cingulate gyrus, and, ultimately,
the neocortex.
• A profound cholinergic deficit, owing to basal
forebrain and pedunculopontine nucleus
involvement, is present in many patients with DLB
and may be a factor responsible for the fluctuations,
inattention, and visual hallucinations.
 MAJOR OR MILD VASCULAR
NEUROCOGNITIVE DISORDER
 MAJOR OR MILD VASCULAR
NEUROCOGNITIVE DISORDER
TYPES :
•Multi-infarct dementia
•Diffuse white matter disease
(also called leukoaraiosis,
subcortical arteriosclerotic
leukoencephalopathy, or
Binswanger's disease)
 MAJOR OR MILD VASCULAR
NEUROCOGNITIVE DISORDER
MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO
TRAUMATIC BRAIN INJURY
 THE LEADING CAUSE OF DEATH IN
PERSONS UNDER 45 YEARS OF AGE IN
THE U.S.
 MORE THAN HALF OF THESE DEATHS
IS DUE TO HEAD INJURIES.
SUBSTANCE / MEDICATION –INDUCED
MAJOR OR MILD
NEUROCOGNITIVE DISORDER
MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO HIV INFECTION
MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO HIV INFECTION
Clinical Findings in the Acute HIV Syndrome
 General
 Fever
 Pharyngitis
 Lymphadenopathy
 Headache/retroorbital pain
 Arthralgias/myalgias
 Lethargy/malaise
 Anorexia/weight loss Nausea/vomiting/diarrhea
 Neurologic
 Meningitis Encephalitis
 Peripheral neuropathy
 Myelopathy
 Dermatologic
 Erythematous maculopapular rash
 Mucocutaneous ulceration
MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO PRION DISEASE
 MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO PRION DISEASE
 FATAL CONDITIONS CHAR. BY ACCUMULATION
OF MODIFIED CELL MEMBRANE PROTEIN (PRION
PROTEIN OR PRP OR PROTEINACEOUS
INFECTIOUS PARTICLE) WITHIN THE CNS
 A SIMILAR CONDITION IN CATTLE (BOVINE
SPONGIFORM ENCEPHALOPATHY) MAYBE A
SOURCE IN MAN
 CREUTZFELDT – JACOB DISEASE
 INCIDENCE : 1 : 1 MILLION
 10 – 15% FAMILIAL
 ONSET : 50 TO 60 YEARS
 NONSPECIFIC SYMPTOMS FOLLOWED BY
ATAXIA, MYOCLONUS, AKINETIC RIGID STATE &
DEMENTIA
 DEATH IN 12 MONTHS
 CSF NORMAL; EEG – HIGH VOLTAGE SHARP
WAVES ON A BACKGROUND OF SLOW WAVE
ACTIVITY
 USUALLY CONFIRMED POSTMORTEM
MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO PRION DISEASE
 MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO PARKINSON’S DISEASE
 MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO PARKINSON’S DISEASE
TREMOR
RIGIDITY
AKINESIA
POSTURAL REFLEX
IMPAIRMENT
Diagram of the basal ganglia in the coronal
plane, illustrating the main interconnections
(see text for details).
 MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO HUNTINGTON’S DISEASE
 HD is a dominantly inherited
disorder characterized by the
gradual onset of motor
incoordination and cognitive decline
in midlife ( an autosomal dominant
disorder caused by mutations in the
IT15 gene that encodes huntingtin)
 MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO HUNTINGTON’S DISEASE

 PATHOLOGY - NEURONAL LOSS

IN THE STRIATUM
 FATAL IN 2 TO 5 YEARS
MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO
ANOTHER MEDICAL CONDITION
MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO
ANOTHER MEDICAL CONDITION
 MAJOR OR MILD NEUROCOGNITIVE
DISORDER DUE TO MULTIPLE ETIOLOGIES
UNSPECIFIED NEUROCOGNITIVE DISORDER
 DERANGEMENTS OF INTELLECT,
BEHAVIOR & LANGUAGE DUE TO
DIFFUSE & FOCAL CEREBRAL DISEASE
 EFFECTS OF
FRONTAL LOBE LESIONS
 Motor abnormalities related to the prerolandic motor
cortex;
 Speech & language disorders related to the dominant
hemisphere;
 Incontinence of bladder and bowel;
 Impairment of certain cognitive functions, especially
attention, concentration, capacity for sustained mental
activity, & ability to shift from one line of thought or
action to another i.e., both impersistence &
perseveration;
 Akinesia & lack of initiative & spontaneity (apathy &
abulia);
 Other changes in personality, particularly in mood &
self-control (disinhibition of behavior);
 Distinctive abnormality of gait
 With regard to the last three of these having
to do with behavior, the anterior half of the
brain is in a general sense committed to the
monitoring and execution of all cerebral
activity. This means that all activities i.e.
motor, cognitive, and emotional are planned
and initiated here. Of necessity in such a
scheme, there must also be inhibitory
mechanisms that control or modulate
behavior.
 Loss of drive
 Impairment of consecutive planning
 Inability to maintain serial relationships of events &
to shift easily from one mental activity to another
 Release (disinhibition) of sucking, grasping, &
groping reflexes and other so-called utilization
behaviors
 Anhedonia (lack of pleasure)
 Apathy
 Loss of self-control
 Disinhibited social behavior
 Euphoria
 EFFECTS OF
FRONTAL LOBE LESIONS
 Contralateral spastic hemiplegia
 Slight elevation of mood, increased
talkativeness, tendency to joke
inappropriately (Witzelsucht), lack of tact,
difficulty in adaptation, loss of initiative
 If entirely prefrontal, no hemiplegia; grasp
and suck reflexes or instinctive grasping may
be released
 Anosmia with involvement of orbital parts
 Left hemiplegia
 Slight elevation of mood, increased
talkativeness, tendency to joke
inappropriately (Witzelsucht), lack of tact,
difficulty in adaptation, loss of initiative
 If entirely prefrontal, no hemiplegia; grasp
and suck reflexes or instinctive grasping may
be released
 Anosmia with involvement of orbital parts
 Right hemiplegia
 Motor speech disorder with agraphia, with or
without apraxia of the lips and tongue
 Sympathetic apraxia of left hand
 Loss of verbal associative fluency; perseveration
 Slight elevation of mood, increased talkativeness,
tendency to joke inappropriately (Witzelsucht),
lack of tact, difficulty in adaptation, loss of initiative
 If entirely prefrontal, no hemiplegia; grasp and suck
reflexes or instinctive grasping may be released
 Anosmia with involvement of orbital parts
 Bilateral hemiplegia
 Spastic bulbar (pseudobulbar) palsy
 If prefrontal, abulia or akinetic mutism, lack of
ability to sustain attention and solve complex
problems, rigidity of thinking, bland affect, social
ineptitude, behavioral disinhibition, inability to
anticipate, labile mood, and varying combinations
of grasping, sucking, obligate imitative movements,
utilization behavior.
 Decomposition of gait and sphincter incontinence
 EFFECTS OF
TEMPORAL LOBE DISEASE
 The special senses (visual,
auditory, olfactory, and gustatory)
 Time perception
 Language
 Memory
 Emotion
 Behavior
 Homonymous upper quadrantanopia
 Wernicke's aphasia (“word-deafness”
;auditory verbal agnosia)
 Amusia (some types)
 Impairment in tests of verbal material
presented through the auditory sense
 Dysnomia or amnesic aphasia
 Visual agnosia
 Occasionally amnesic (Korsakoff) syndrome
 Inability to judge spatial relationships in
some cases
 Impairment in tests of visually presented
nonverbal material
 Agnosia for sounds and some qualities
of music
 Auditory, visual, olfactory, and gustatory
hallucinations
 Dreamy states with uncinate seizures
 Emotional and behavioral changes
 Delirium (usually nondominant)
 Disturbances of time perception
 Korsakoff amnesic defect (hippocampal
formations)
 Apathy and placidity
 Hypermetamorphopsia (compulsion to
attend to all visual stimuli), hyperorality,
hypersexuality, blunted emotional
reactivity (Kluver-Bucy syndrome; the full
syndrome is rarely seen in man)
 EFFECTS OF
PARIETAL LOBE DISEASE
 Corticosensory syndrome and sensory extinction (or total
hemianesthesia with large acute lesions of white matter)
 Mild hemiparesis (variable), unilateral muscular atrophy in
children, hypotonia, poverty of movement, hemiataxia (all
seen only occasionally)
 Homonymous hemianopia or inferior quadrantanopia
(incongruent or congruent) or visual inattention
 Abolition of optokinetic nystagmus with target moving
toward side of the lesion
 Neglect of the opposite side of external space (far more
prominent with lesions of the right parietal lobe)
 Disorders of language (especially alexia)
 Gerstmann syndrome (dysgraphia,
dyscalculia, finger agnosia, right-left
confusion)
 Tactile agnosia (bimanual astereognosis)
 Bilateral ideomotor and ideational apraxia
 Visuospatial disorders
 Topographic memory loss
 Anosognosia, dressing and constructional
apraxias (these disorders may occur with
lesions of either hemisphere but one
observed more frequently and are of greater
severity with lesions of the nondominant one)
 Confusion
 Tendency to keep the eyes closed, resist lid
opening, and blepharospasm
 Visual spatial imperception, spatial
disorientation, and complete or
partial Balint syndrome (optic
apraxia)
 EFFECTS OF
OCCIPITAL LOBE DISEASE
 Contralateral (congruent) homonymous
hemianopia, which may be central
(splitting the macula) or peripheral; also
homonymous hemiachromatopsia
 Elementary (unformed) hallucinations
usually due to irritative lesions
 Right homonymous hemianopia
 If deep white matter or splenium of
corpus callosum is involved, alexia and
color-naming defect
 Visual object agnosia
 Left homonymous hemianopia
 With more extensive lesions, visual
illusions (metamorphopsias) and
hallucinations (more frequent with
right-sided than left-sided lesions)
 Loss of topographic memory and visual
orientation
 Cortical blindness (pupils reactive)
 Anton syndrome (visual anosognosia,
denial of cortical blindness)
 Loss of perception of color
(achromatopsia)
 Prosopagnosia (temporo-occipital),
simultanagnosia (parieto-occipital)
 Balint syndrome (parieto-occipital)
DISTURBANCES OF THE NONDOMINANT
CEREBRAL HEMISPHERES
DISCONNECTION
SYNDROMES
 Result when the entire corpus callosum is destroyed
by tumor or surgical section.
 The language and perception areas of the left
hemisphere are isolated from the right hemisphere.
 Patients if blindfolded, are unable to match an
object held in one hand with that in the other.
Objects placed in the right hand are named
correctly, but not those in the left.
 If rapid presentation is used to avoid bilateral visual
scanning, such patients cannot match an object
seen in the right half of the visual field with one in
the left half.
 Alexia in the left visual field, since the verbal
symbols that are seen there and are
projected to regions of the right hemisphere
have no access to the language areas of the
left hemisphere
 If given a verbal command, such patients will
execute it correctly with the right hand but
not with the left; if asked to write from
dictation with the left hand, they will produce
only an illegible scrawl.
 Conduction aphasia
 Ideomotor apraxia in Broca's
aphasia
 Pure word-deafness
 SPECIAL
NEUROPSYCHOLOGIC TESTS
 Milan Sorting Test, Halstead Category Test,
and Wisconsin Card-Sorting Test as tests of
ability to abstract and shift paradigms
 The Porteus Maze Test, Reitan Trail-Making
Test, and the recognition of figures in the
Figure of Rey as tests of planning, regulating,
and checking programs of action
 Benton's Verbal Fluency Test for estimating
verbal skill and verbal regulation of behavior
 Figure of Rey, Benton Visual Retention Test, Illinois
Nonverbal Sequential Memory Test, Recurring
Nonsense Figures of Kimura, and Facial Recognition
Test as modality-specific memory tests
 Milner's Maze Learning Task and Lhermitte-
Signoret amnesic syndrome tests for general
retentive memory
 Seashore Rhythm Test, Speech-Sound Perception
Test from the Halstead-Reitan battery,
Environmental Sounds Test, and Austin Meaningless
Sounds Test as measures of auditory perception
 Figure of Rey, Wechsler Block Design and Object
Assembly, Benton Figure Copying Test, Halstead-
Reitan Tactual Performance Test, and Fairfield Block
Substitution Test as tests of constructional praxis
 Several mathematical and logicogrammatical tests
as tests of spatial synthesis
 Cross-modal association tests as tests of
suprasensory integration
 Benson-Barton Stick Test, Cattell's Pool Reflection
Test, and Money's Road Map Test, as tests of spatial
perception and memory
 Color naming, color form association,
and visual irreminiscence, as tests of
visual perception; recognition of faces of
prominent people, map drawing
THANK YOU