NEUROPSYCHOLOGY

UPDATE

Emotional

and Cognitive Correlates of Multiple Sclerosis Roberta

Firnhaber

T

his talk focuses on multiple sclerosis (MS), one of several diseases in which the myelin sheaths of the nerve fibers are destroyed. MS is a disorder of the central nervous system (CNS) and can affect any part of the CNS, including the lum, the spinal

optic cord,

nerves, the the subcortical

brain

stem, the white matter,

cerebeland the

At autopsy, MS lesions-called plaques-in the brain and spinal cord have a pinkish-gray color and are sharply delineated. They are frequently distributed randomly in the brain stem, spinal cord, and cerebellar peduncles. MS also frequently attacks the optic nerves and chiasm, but usually not the optic tracts. cortex.

In

the

brain,

MS

plaques

tend

to cluster

around

the

veins lining the lateral ventricles, producing a high proportion of lesions in periventricular white matter. Cortical lesions show destruction of myelin, but nerve cells are left essentially intact. It is believed that remyelination occurs at times, accompanied by associated changes in magnetic resonance imaging of the lesions.’ Two-thirds of patients with MS have onset between the ages

of 20 and

40. MS is much

more

common

in women

than

in men (ratio of 1.7:1). Early symptoms of MS inweakness in one or more limbs reported by about 50% of patients, and retrobulbar or optic neuritis, reported by 25% of patients. Retrobulbar or optic neuritis involves partial or total loss of vision, usually occurring dude

over

several

hours

or days.

A variety

of other

symptoms,

occurring either singly or in groups, may herald the onset of MS. They include nystagmus, ataxia, diplopia, hemiplegia, vertigo, seizures, deafness, facial paralysis, unformed auditory hallucinations, aphasia, and emotional changes. A long latency period, as long as 10 years, may follow

422

SERIES

White,

Ph.D.

an initial

symptom.

the periods

Generally,

of remission

as the disease

become

shorter.

progresses,

The

relapse

rate

is about .3-.4 exacerbations per year, although the interval between relapses ranges widely. McAlpine and Compston found that 30% of patients they studied reported between-relapse intervals of 1 year; 20% reported intervals of 2 years; 10% reported intervals of 5-9 years; and 10% reported intervals of 10-30 years.2 Adams and Victor3 noted a relationship nancy and increased exacerbations. Other reported a temporal relationship between and

subsequent

exacerbations

cumulative

of MS

number

is extremely

viral

preghave

infections

of MS.4

As the disease progresses, period of deterioration that to the

between workers

patients

tend

Adams

and

of CNS

lesions.

variable,

to enter

Victor3 The

ranging

from

a

attribute duration months

to

many years, with average duration greater than 30 years. Based on its clinical course, MS is sometimes characterized as either chronic-progressive, remitting or relapsing, or acute

(rapidly

progressive).

MS patients tend to fall into one of four subtypes. About 50% of MS patients have a mixed or generalized type, which involves the optic nerve, the brain stem, the cerebellum, and the spinal cord. Another 30% to 40% have

a spinal

each

have

of MS, a cerebellar

(optic

nerve)

amaurotic Address

form

either

reprint

requests

and

about

5%

or pontobulbar

of MS

patients

form,

or an

form.

to Dr. White,

Boston

Veterans

Administration

Avenue, Jamaica Plain, MA 02130. This paper is based on a talk given at the Institute of Living Symposium on the Neuropsychology of Neurobehavioral Disorders, held October 29, Hospital,

1988,

150 South

in Hartford,

Copyright

Huntington

Connecticut.

© 1990

American

Psychiatric

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NEUROPSYCHOLOGY

No known treatment reverses MS or halts the associated process of demyelination. Although some experimental treatments based on immune system theories of MS exist, the disease is usually treated symptomatically using adrenocorticotropic hormone (ACTH), a pituitary hormone that stimulates the adrenal glands, or prednisone.

GENETICS

AND

UPDATE

SERIES

the South.5 In addition, Ebers9 has reported that siblings tend to develop MS during the same calendar year, not at the same age, suggesting an environmental influence. The nature of the mechanism of environmental influence on the development of MS has received much discussion. It has been argued that viral infections occurring early in life later produce an autoimmune response that in turn triggers the demyelinating exacerbations of MS.’#{176}

EPIDEMIOLOGY

NEUROPSYCHOLOGY OF MS The cause of MS remains a mystery, but considerable A considerable literature exists on the cognitive, affecresearch indicates that its development may be related to genetic, environmental, and immunologic variables. Sevtive, and personality correlates of MS. Taken as a group, however, the studies eral investigators have re ported a distribution of completed to date are difMS cases related to latificult to interpret because Dr. White’s article is the fourth and final in a series on neuropsytude of residence. In gennearly all treat MS as a chological testing. The first article, by Dr. Edith Kaplan (Winter eral, MS is more common unitary disorder. As we 1990), presented a process approach to neuropsychological assesshave already seen, that is in northern latitudes. ment. In the second article of the series (Spring 1990), Dr. GeralKurtzke and co-workers5 a remarkable oversimplidine Cassens et al. discussed neuro psychological evaluation of reported prevalence rates fication. MS lesions can depressed patients. In the previous issue (Summer 1990), Dr. for MS of I per 100,000 in occur in several parts of Larry J. Seidman discussed the neuro psychology of schiwphrenia. the CNS, a tendency that equatorial areas, 6-14 per All of these articles are based on talks presented at a symposium on the neurobiology of neurobehavioral disorders, held at 100,000 in the southern suggests that, behaviorthe Institute of Living in Hartford, Connecticut. Together, they ally, there may be several U.S. and in southern Eurepresent part of an ongoing effort by The Journal of Neuropsysubtypes of neuropsyrope, and 30-80 per chiatry and Clinical Neurosciences to feature comprehensive 100,000 in Canada, northchological dysfunction in reviews of the latest diagnostic technologies available to neuroMS. depending on the ern Europe, and the psychiatrists. northern U.S.____________________ ________________________ sites of focal lesions in inIn addition, it has been dividual cases. Given this noted that people who move from high-risk latitudes to proviso, I review the literature on cognitive, affective, low-risk latitudes carry with them some of the risk of and personality effects of MS. their place of origin, at least if immigration occurs after MS and Cognition age 15.6 Epidemiologic investigations have also shown evidence of “epidemics” of MS.7 Most investigators agree that visuospatial and visuomoThere is also evidence to suggest that there may be a tor impairments occur in MS.”-’6 It seems likely that this genetic component to susceptibility to MS. The risk of MS consistency in findings reflects the multiplicity of MS is 15 to 20 times greater in first-degree relatives of affected lesion sites that produce visuospatial loss (e.g., optic individuals, and the highest risk appears to be among nerves, white matter, and cerebellum). Similarly, virtually all studies of short-term memory in siblings. Twin studies are fraught with methodological problems but suggest overall that MS affects both twins MS have reported memory deficits. Deficits have been more frequently in monozygotic than in dizygotic diads.9 reported on several types of tasks,’7”8 including the The patterns of MS development in genetic studies sugWechsler Memory Scale,’9’2#{176} the Rey Auditory Verbal Learning Task,’9 the California Verbal Learning Test, and gest multigenetic influences, rather than single-gene the Spatial Recall Test.21’22 Memory impairment on both transmission.9 recall and recognition memory tasks has been described’5 Many workers favor theories of MS etiology that combine genetic and environmental factors. This notion reand has been ascribed to a general problem in cognitive inefficiency or to frontal lobe dysfunction.2’ Again, it ceives support from evidence that racial differences in the prevalence of MS are nonetheless affected by the latitude appears likely that memory problems may be ubiquitous of habitation. In the U.S., for example, blacks have lower in cerebral forms of MS. However, the underlying neurates of MS than whites, but blacks living in the northern ropathological and associated functional explanation of U.S. are more likely to develop MS than blacks living in the etiology of observed memory loss probably varies a -________________________

Neuropsychology

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NEUROPSYCHOLOGY

great

deal

UPDATE

among

MS plaques

patients

and

compared IQ scores

without aulo

with in MS

MS who

had

et al.27 reported

scores Several

(less

than other

cases

reflects

different

sites

of

of cases. Results of studies of the effects of MS on intellectual performance, attention, abstraction and reasoning, and verbal and language ability have been contradictory. The first psychometric study published on MS dates to 1921, when Brown and Davis concluded that there may be intellectual decline in MS, although their measures were unable to detect any.24 Diers and Brown,1’ in 1950, reported lowered scores on several Wechsler-Bellevue subtests (Digit Spans, Block Designs, Object Assembly, and Digit Symbol) relative to norms, but they concluded that these results could be attributed to motor impairment and anxiety rather than to true intellectual loss. Other investigators have reported verbal intellectual loss’2 and lower IQ scores22 on the Wechsler Adult Intelligence Scale (WAIS)’2 and on the German IQ tesP among MS patients lower

in individual

SERIES

normal patients other

or groups

controls. compared

neurological

abnormal

Ivnik’6 with

reported subjects

disorders.

Mini-Mental

State

DePExam

24) in 14% of MS patients. workers,

however,

reported

no evidence

of intellectual decline on the WAIS scales in MS patients compared with normal controls’7”9’2#{176}or with other neurologic or non-neurological patient groups.’4”7’2#{176}Raven’s scores in MS patients and normal controls have also been reported Reports

to be similar.2#{176} of impaired

performance

on the

Digit

Span

in

MS patients have emanated from at least three studies.27’28 Yet, other investigators have reported no attentional problems26 on Digit Spans’9 or other tasks such as Continuous Performance Tests.2”22 In one study, Paced Auditory Serial Arithmetic Test (PASAT) performance of MS patients was impaired at the two highest speeds,’9 suggesting that when tested for limits, MS patients may show impaired attentional capacity on complex tests. Fink and Houser22 reported impaired performance on the WAIS Similarities and Comprehension Test in MS patients when compared to normal controls. Others have reported normal performance on the WAIS verbal reasoning subtests in MS patients.”7”9 Goldstein and Shelly’4 found that MS patients perform similarly to other brain-damaged patients and neuropsychiatric patients on WAIS Similarities and Comprehension Tests. Heaton et reported impaired performance on the Halstead-Reitan Categories Test in patients with chronic progressive, but not relapsing or remitting, MS. Similarly, Peyser et al.29 reported that 50% of MS patients in their sample had abnormal performance (i.e., error scores greater than 50) on the Categories Test. Parsons et al.3#{176} reported impaired abstraction in MS patients on a reasoning test using blocks, after controlling for other pos-

424

sible

sources

of error,

such

as attention.

Conflicting reports in findings reflect variations in the disease thing

on abstract abilities process more than

may any-

else.

Goldstein and Shelly’4 reported sample of MS patients compared

intact verbal skills with neurological

neuropsychiatric

MS has

control

subjects.

been

in a and

described

as a “subcortical” dementia characterized by intact verbal abilities relative to visuospatial and memory skills.22 However, several investigators have nonetheless described verbal and language loss in MS patients. Deficits have been reported on the WAIS vocabulary test,”6 naming,17’22 reading,’7 and verbal fluency.’2 Again, the discrepancies in findings on verbal dysfunction in MS most likely reflect the variability of MS lesion sites in the MS samples used by different investigators. They also reflect differences in the control groups used in the studies. For example, Goldstein and Shelly,’4 who compared MS patients to patient groups likely to show cognitive loss (neurological patients and neuropsychiatric patients), would be expected to find fewer effects of MS than researchers who compared MS patients with normal control subjects. Because MS can extensively affect subcortical white matter, thus interrupting connections to cortex, and because MS lesions can be found in the white matter in cortex, it is reasonable to conclude that some MS patients will exhibit naming deficits and other symptoms of language loss. Disease Variables Some researchers have investigated whether specific types of changes in cognition are related to variations in the MS disease process or variations in the effects of the disease. Disability tients verbal

These rating.

studies

Fink

are

discussed

and

below.

Houser22

with greater disabilities showed subtest scores on vocabulary,

reported

that

lowered similarities,

pa-

WAIS and

comprehension. However, Marsh3’ found no relationship between severity of disability and degree of intellectual decline. It is easy to explain such divergent findings by considering the issue of lesion site: the patient with spinal cord or optic nerve involvement might be severely disabled physically but have little or no cerebral demyelination and thus show little intellectual loss. Duration of MS. Studies have yet to show any direct relationship between length of illness and degree of deterioration in neuropsychological functioning.’6”8’26 Degree of cerebral demyelination would appear to be a more powerful predictor of neuropsychological decline than duration of illness.

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Type

of MS.

Heaton

sive

patients

were

ting

patients

on

et al.’2

impaired

a wide

variety

tests. However, Raymond between chronic-progressive mitting

patients

Test, Clinical that

on

or spatial

exams.

examinations

that

chronic

than

relapsing-remit-

progres-

of neuropsychological

et al.Zl’22 found no differences patients and relapsing-re-

the

recall

medical

clinical

found

more

CVLT,

CPT,

Letter

Cancellation

tests. It has been consistently underestimate the

cognitive loss found on neuropsychological in MS patients’2 or even on quantitative simple as the Mini-Mental State Exam.32

reported degree of

test batteries measures as

Exacerbation. Exacerbation status is a potentially powerful but often unaddressed variable affecting neuropsychological function in MS patients. Because clinical studies rely on hospitalized patients for their subjects, patients hospitalized for acute exacerbations may be overrepresented in clinical studies on MS. In the opinion of this author, underlying neuropathology is the most important variable to study when addressing the question of cognitive changes in MS. It was, of course, very difficult to do such studies in the early years of interest in MS, when imaging techniques were either unavailable or insensitive to MS. Neuropathology.

Thus, sites

autopsy reports with behavioral

were deficits.

needed Such

to correlate reports still

left

lesion a lot

of unanswered questions about deficits in the early stages of the illness, when fewer lesion sites and more focal findings would be expected. Computed tomography scans appear to be less sensitive to MS lesions than magnetic resonance imaging, and a patient with a negative CT scan may show lesions on MRI. However, CT scanning at times detects MS lesions and can be used to estimate the degree of cerebral atrophy. In a study published in 1986, Jennekens-Schinkel and Sanders33 summarized CT scan behavioral data on three MS patients. One patient showed slowing, but relatively intact, cognitive functions; her CT scan revealed multiple white matter lesions, but no atrophy. The two other patients, who had marked cognitive decline, showed white matter lesions plus underlying atrophy on CT, suggesting that atrophy may be an important cause of global cognitive loss in MS. Rao et al.’8 examined neuropsychological and CT data on 47 patients with chronic progressive MS. They found that increased size in the third ventricle, but not bifrontal or bicaudate spans, were related to decreased cognitive function on intellectual and memory tests. They theorized that the loss seen in function may be due to disruption of fiber tracks to prefrontal limbic structures by

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plaques in the periventricular white matter surrounding the third ventricle. The ideal study would longitudinally use MRI scanning and neuropsychological testing to correlate development of lesions with changes in cognitive function. In addition, longitudinal prospective study of the physical symptoms of MS and corresponding changes in neuropsychological function could provide a great deal of information about the neuropsychology of MS. Even without such studies, it is possible to predict with a reasonable degree of accuracy the type of behavioral deficits that could be associated with each of the usual MS lesion sites. Lesions of the spinal cord are expected to produce sensory or motor deficits on neuropsychological evaluations. Since such lesions are found in 30% to 40% of all cases, the single finding of sensory or motor loss in a patient may suggest this lesion site. Optic nerve involvement would produce visuospatial deficits on neuropsychological testing. A clinical case example of this neuropsychological optic spinal

nerve cord

lesion

site is a 39-year-old patient seen for testing. Her neurologist diagnosed

involvement involvement.

leg

numbness,

heat,

and

with questionable Physical symptoms

diminished

left

optic

coordination,

neuritis.

cerebellar included

or

sensitivity

Neuropsychological

to testing

showed impairment on the Digit Symbol and Picture Arrangement subtests of the WAIS-R. Lesions in the brain stem would be expected to produce attentional deficits on neuropsychological testing. Cerebellar

lesions

are commonly rience with with

MS

that MS visuospatial The

often

result

in writing

seen in MS. In addition, other types of cerebellar

patients

with

patients with deficits.

presentation

cerebellar lesions

deficits,

involvement, in

this

suggests

site

of neuropsychological

demonstrate deficits

tients with subcortical white matter involvement to occur on a continuum. In the early stages, number mild

of lesions deficits

Paced Card

is relatively

on

Auditory Sorting

In the

more

executive Serial

which

our clinical expelesions, as well as

slight,

patients

function

often

tasks,

Addition

Task

stages,

patients

in pa-

appears when the such

and

show as

the

Wisconsin

Test. moderate

may

show

the

classic pattern of “subcortical dementia,” characterized by visuospatial impairment, difficulty with anterograde memory, and intact language. In this category was a 39-year-old male attorney with spinal, optic, and white matter signs on neurological examination. He had been diagnosed with MS 8 years prior to evaluation. Leg numbness, diplopia, and impaired gait were reported. His neuropsychological testing showed that language skills, with the exception of verbal fluency, were intact.

425

UPDATE

NEUROPSYCHOLOGY

He

had

zation.

difficulty Motor

with speed

visuospatial was

impaired.

SERIES

analysis He

and was

organifound

Emotional on

short-term memory testing to be sensitive to interference when attempting new learning. Behavior and personality style were highly repressed. As the disease progresses and the involvement of subcortical white matter becomes more widespread, a picture of diffuse cognitive change, with all types of cognitive problems, emerges. These include difficulties with naming, general language, visuospatial skills, and memory. One patient with this pattern of performance, a high-functioning systems analyst with 17 years of education, was seen on two occasions, once in 1982 and again in 1986. In 1982, at the time of her third MS exacerbation, she was evaluated for complaints of cognitive changes. Her MS symptoms included visual field loss in the right center and left side. Neuropsychological test results showed a verbal IQ of 129. However, performance IQ was 99. Motor slowing, impaired motor coordination, mild problems with short-term memory, fatigue, anxiety, and depression were all observed. In 1986, her verbal IQ was 128 and performance IQ was 93. However, she had shown a decline in performance on Digit Symbol, Picture Arrangement, Picture Completion, and Delayed Recall anterograde memory tests. Memory quotient declined from 125 to 118. Likewise, she showed increased word-finding difficulty on the Boston Naming Test, but she did not make verbal paraphasic errors. Cognitive inflexibility was seen on testing on the Wisconsin Card Sorting Test, and her score on the Benton Recognition Memory Task had declined. In addition, she reported greater symptoms of depression in 1986 than in 1982. Focal cortical lesion sites can be observed on CT or MRI, with associated focal neuropsychological test findings. Thus, a patient with lesions predominantly in frontal or parietal areas would be expected to demonstrate the usual pattern of focal cognitive changes associated with that lesion site. One such patient, a 28-year-old, right-handed female college graduate who had studied early-childhood education, was seen by the author 2 years after her symptoms began. Early symptoms consisted mostly of optic neuritis and incontinence. Behaviorally, she showed depressive symptoms, and each of her several exacerbations began with suicidal ideation. Her neuropsychological test results were overall normal quantitatively. However, consistent qualitative evidence of frontal lobe dysfunction was seen, including perseverative contamination on Visual Reproductions, tremor with the left hand, closing in on drawings to copy, losing set on the Wisconsin Card Sorting Test, and sensitivity to interference on memory tasks. MRI showed deep frontal and cerebellar lesions.

426

Changes

and

Psychiatric

Symptoms Psychiatric

since

changes I 800s

in MS patients by such eminent

the early

have been observers

last 40 years, disturbances health and

Charcot and Vulpian. In the have reported psychological variety of measures of mental

reported of MS as

many

workers

in

MS on described

have

a

of different types of psychiatric disturbances in MS patients?US Harrower and Kraus described personality traits believed to be typical of MS, and some a number

workers

have

illness.

Basically,

around psychotic

theorized

hysterical symptoms.

work

that on

MS the

symptoms,

may

be a psychological

psychiatry

of MS

affective

disorders,

centers and

Early reports that MS patients have hysterical personality styles later received possible support from studies using the Minnesota Multiphasic Personality Inventory. These studies consistently showed elevations on scales 1, 2, and 3 of the MMPI, the so-called “neurotic triad” of hysteria, hypochondriasis, and depression.’3’7 Some theorists have interpreted these findings as a reflection of a hysterical premorbid personality style in MS patients, while others have seen them as evidence of organic personality and affective disorders secondary to MS. Interestingly, Ross and Reitan’3 also found elevations on scales 1,2, and 3 in other brain-damaged patients and normal controls. Matthews et al.39 reported higher rates of abnormal MMPI profiles in MS patients than in a control group of patients with other types of brain damage. Peyser et al.4#{176} described five types of MMPI profiles in a sample of MS patients. They reported that the classic 1,2,3 pattern usually occurred in patients who had relatively intact cognition, but moderate physical disabilities. Patients scoring high on scales I and 3 and lower on scale 2 had intact cognition but few physical symptoms. Patients who were high on scale 8 tended to show a great deal of cognitive loss. These classic MMPI profiles bring up a thorny problem in neuropsychological differential diagnosis: distinguishing between hysteria and early MS. One patient seen for this differential diagnostic question was a 48year-old, right-handed male who clearly had MS and who had marked deficits on neuropsychological tests. He had a verbal IQ of 95, a performance IQ of 77, and a Memory Quotient of 77 on formal testing. He also showed impaired naming with paraphasic errors. His MMPI profile (scores above 70 on L and K and elevated scores on scales 1, 2, and 3) was considered to be classically “hysterical.” Another patient seen for the same differential diagnosis was a 29-year-old left-handed woman with a similar MMPI profile. Neuropsychological test scores were all in Hysteria.

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the low-average to borderline range. Her only unusual findings were bimanual tremulousness in drawing and writing and complaints of fatigue on mood assessment. CT scan suggested left basal ganglia lesion, but M, CSF studies, and evoked potentials were all normal. Given the difficulty of diagnosis in the early stages of MS. the number of MS patients whose initial diagnoses were hysteria, and the possibility that the patient suffered from another noncerebellar form of MS. the neuropsychologist did not come to a definite conclusion in regard to the diagnosis of MS. However, it was concluded that the patient had likely had a congenital or early developmental injury resulting in current personality problems. syndromes. Affective symptoms have been described repeatedly in MS. The symptom of euphoria was one of the earliest psychiatric symptoms decribed in MS patients, but there has been disagreement about whether MS patients are euphoric in the clinical sense of hypomania or mania or only show inappropriate lack of concern regarding their health. It is generally agreed, however, that affective syndromes occur in MS. Cottrell and Wilson,4’ in 1929, reported that 84% of their patients were “abnormally” optimistic; 10% were depressed; and 63% were euphoric. Surridge35 reported a high incidence of euphoria but not depression in MS. In contrast, Joffe et al.42 reported recurrent depression in 42% of their MS patients and bipolar disorder in 13% (the rate of bipolar disorder in the general population is 1%). Schiffer et al.,43 in an epidemiological investigation, reported that concurrent diagnoses of affective disorder and MS were found twice as often as would be expected based on the population rates of the two disorders individually. Although a few reports have looked at the relationship between imaging studies and affective symptoms, two reports could find no association between CT lesion sites and affective complaints.42’43 A study of eight patients with psychiatric disorder (four with depression, two with bipolar disorder, and two with organic personality disorder), however, showed a preponderance of temporal lobe lesions on MRI.”’ There are several case reports of onset of MS characterized by manic episodes.47 In addition, a neuropsychological evaluation was conducted by this author on a 27-year-old, right-handed college graduate with a history of mania whose MS symptoms began four years prior to testing and included ataxia and tremor of the right hand. At the time of evaluation he had optic neuritis. He had had a manic episode with a great deal of spending and hyperactivity two years prior to evalua-

Affective

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tion. At evaluation, he showed widespread neuropsychological deficits. Verbal IQ at the time of evaluation was 91, and performance IQ was 64. Wechsler Memory Quotient was 77, and confrontation naming of pictures of objects was significantly impaired. Bipolar” and depressive syndromes have also been described in MS. I have seen several patients with MS whose most troublesome symptom was depression. The depression interfered with correct diagnosis of the patients’ actual problem. For example, one patient had been hospitalized for 15 years and had undergone ECT several times before MS was diagnosed and determined to have been quite long-standing. Another patient with a preexisting diagnosis of depression experienced intensification of depressive symptoms as his MS progressed. In a third patient, suicidal ideation was probably the initial symptom of MS. Formal psychiatric symptoms have also been reported in MS. Several investigators have diagnosed schizophrenia in MS patients, usually using the term to describe an apathetic state.4#{176} There are also reports of hallucinations and delusions in MS. One such patient whom I had seen for neuropsychological evaluation was a 51-yearold right-handed nurse with 15 years of education who showed hallucinosis during exacerbations. Five years prior to evaluation she had shown symptoms of lefthanded numbness that lasted a few days. Ten months prior to my evaluation, she suffered right leg weakness. She had been experiencing symptoms of hyper-religiosity for 6 months, and insisted that God talked to her and that she had seen a burning cross in the sky. Her neuropsychological testing showed an IQ of 88. Premorbid IQ was estimated to have been greater than 100. Specific problems were observed on visuospatial tasks, including occasional left inattention and inability to draw in perspective. Her performance on similarities and visual memory were impaired, and she showed impaired verbal fluency. She was remarkably “pulled” to stimuli on visual constructive tasks. Her MMPI profile, however, was normal. CT scan revealed a right frontal lesion. Neuro pathological correlates of mood and personality change. Although it seems likely on the face of it that mood and behavioral changes occurring in MS should be definable in terms

of brain-behavioral

develop

a theory

linking

It is possible elusive than

that the

come. more they

are

not

structurally

relationships, lesion

site

and

it is difficult personality

to out-

the emotional sequelae of MS are cognitive changes of MS in that hard-wired,

but

are

related

to

autoimmune or neurochemical processes. This is yet another of the many frontiers remaining in the effort to understand the behavioral anomalies that occur in MS.

427

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