Cognitive impairment in the elderly diabetics

Arch. Gerontol. 0167-4943/96/$15.00

Geriatr. 0

auppl. 5 (1996) 1996 Elsevier

COGNITIVE

IP~!PAIRMENT

M.

MOTTA,

S.

G.

SEMINARA

Institute Cannizzaro,

SORACE, and

of

P.

43-46 Science

IN

Tj1E

S.

RESTUCCIA,

Ireland

ELDERLY

Ltd. All rights

43

reserved

DIABETICS

G.

CARNAZZO,

G.

CORRAO,

MAUGERI

Internal Medicine and Geriatrics, Via Messina, 829, l-95126 Catania,

Catania Italy

University,

Ospedale

SUMMARY In the elderly patients, cognitive impairment is often associated with especially with memory loss. The underlying mechanism of this phenodiabetes, Metabolic changes can play an important role, menon have not been cleared up. because either low or high blood sugar levels can affect the cognitive performance. Here we report our preliminary data from an ongoing study on cerebrovascular deficits in diabetic elderly patients. Keywords hyperglycemia

: senile

diabetics,

aged

diabetics,

cognitive

impairment,

hypoglycemia,

INTRODUCTION Diabetes cosuria, affects of

is a dysmetabolic

causing the

central

flow

can

permanently

and

behavioral

1990)

in

and

damage

lesions

atrophy,

neuropathy

gical

of

and be

in

grey

disorders the fact, not stract an

causal the clear.

been

could

studies

be

connected

with

relationship specific The

and role

in

reported,

phenomena.

cerebral in

observed

psychomotor these

been

the

of

decline

in

diabetics

with

and

peripheral

CNS.

by

However,

neuropsycholo-

and

difficult

diffuse

white various

to establish

diabetic

of cognitive involve

Neu-

Although,

is in

al.,

characterized

encephalopathy.

it

Metabolic

et

plaques.

the

1965).

deficits

the

performance.

of

confirmed

al.,

agents

neuropathy

angiopathy

have

involved

disorders

fibrosis,

cerebral oral

(Dejgaard

patients

diabetic

et

diabetes

or

are

lesions

not the

alters

risk

neurophysiological

presence

also are

meningeal

and insulin

peripheral

diabetic

(Reske-Nielsen

underlying

mechanisms main

the

present

with

the

authors

with

that

pictures

increases

encephalopathy,

and

correlated

reported

degeneration

Some

diabetics

indicate

these

brain,

glu

Diabetes

it

with

and

damages.

neurochemical,

diabetic

may

that

the

observed.

dilatations

hyperglycemia

tissue ways:

including

in

called

study

matter

reasoning important

this

mind

which

ropathological and

lesions

various

Cerebral

CNS

microangiopathy

kept

deficits

the

and

overtreatment

brain.

ventricle

results

beds

have of

in

eventual

the

These

cerebral

must

an

by

organ

(CNS)

vascular

modifications

described

The

it

all

characterized

functional

system

metabolism;

microangiopathy. by

and

nervous

atherosclerosis

blood

syndrome

structural

subjects. performance

memory changes

are

recall, seem

In

to

abplay

44 THE

METABOLIC The

ses

ALTERATIONS

brain

requires

a decline

in

hypoglycemia

are

havioral

type

range

(Ryan

voke

cognitive

cortex,

striatum

cerebral

capacity

ported.

In

ration,

and

hyperglycemia

is

obtained

so

correlation

between

the

impaired

memory

far

as

have

revealed

neuronal

the

normal

may

pro-

necrosis

in

the

the of

onset

on

are

conflicting. deficit

and

brain

Some

as

in

the

is

have

of

in

reaction

alte-

not

of hy-

observed

learning,

times

clear

biochemical

while

difficulty

re-

not

episodes

hyperglycemia,

such

responses

kind during

authors

been

metabolic It

what

et al.,

have

evident

alterations

and

[Cold

1992)

more

be-

intellectual

attention

al.,

complications.

performance

cognitive

poor

et

in

data

a correlation Reduced

and

(Draelos

represents

performance,

and

such

concentration

relevant

The

cerebral

disorders

to

of

neurobe-

hypoglycemia

alterations.

fluency

brain

responsible.

perglycemia

ported

reduced and

influences

are

metabolic

hyperglycemia

hyperglycemia

mechanisms

subjects

and

memory

diabetes,

the

returns

of

cau-

episodes

hippocampus.

19911,

verbal

depletion

that

glycemia

episodes

damages,

hypoglycemic

et al.,

impaired

how

and on

provided

when

repeated

glucose

accompanying

character

cerebral

deterioration

(Langan

1994),

and

and

changes

reestablished

However,

disorders

correctly

transient

are

1993).

studies

function Cerebral

of

performances

corpus

to

function.

considered

et al.,

Various tween

glucose

neuronal

any

others

re-

short

term

[ Reaven

et

al.,

1990).

DIABETES

AND

ACING

Diabetes cing

years,

as

reported age

(Wilson

rioration

the et

in

are

elderly

subjects after

“senile type

II

have

on

related diabetics

with

the are

opinion

which

has of

age

by played

gets

of

diabetes

the

duration

aging

increase The

over since

understanding

mechanism

with

advan-

Framingham

subjects

consideration,

A deeper the

diabetes

role

patient onset

aging.

study

65

years

cerebral of

underlying

process,

developing

of

in

characteristics.

developed

diabetic

the

12 % in

merit

temporary

The

the

frequency studies.

was

data

reveal

that

only

diabetes”.

with

its

the

the

of dete-

aging

pro-

cerebral

defi-

subjects.

not

years

and

diabetes

These

may

aging

epidemiological

of

1986).

diabetic

70

to

various

patients

of

which

by

correlated

diabetic elderly

We

related

prevalence

al.,

is also of

liarities

self

closely shown

that

cess cits

is

in

calling

the

by

older,

middle

must

mellitus? disease, characterized

from “aged what

i.e., be

In the

age

former

aging,

advanced

considered.

aged type by

ages

We distinguish

diabetics, of

treatment

generalized

diabetes diabetes” happens What the

has

pecu-

diabetes

in

manifesting and and a role

the how

aging.

and

regional

latter when

can

pathology

and

it-

aging is

In

corsenile

athero-

a

45 arterio-sclerosis, the

tissue A

of

is utilization

of

longitudinal

diabetes

by

and

can

tics,

by

and

The

diabetics

years);

(ii)

Table

Mini

(onset

(iii)

controls

in

Table

I.

AND

THE

with

years

prolonged

may

duration

also

co-existing

[MMSE)

(Brink

be

explained

vascular

disea-

elderly

diabe-

of

age,

46 years, 73.36

age

into

at

mean

+ 5.78

et

al.,

1975)

1982).

divided

mean

in

(Folstein

et al.,

were

at age

diabetes.

impairment

Examination (CDS)

(onset

that

cognitive

damage,

(mean

Parameters Age range Number of Number of scores males females

CDS

scores males females

Notes:

the

age

three

groups:

study: at

years).

76.47

the

The

(i) -+ 4.51 74.30 -+

study: observations

tistically

signififcant These aged

The

are

betes the

can

female data

STDUY

Aged

GROUPS

diabetics

(means

will

Controls

66 - 83 15 8

65 - 84 15 15

25.30 27.87 23.93

+ 4.31 T 0.99 T- 4.78+

26.33 25.80 24.09

+ 4.11 T 0.79 ?- 0.46

16.26 17.84 15.33

+ 6.69 7 6.21 T- 6.18

18.91 22.00 17.26

+ 5.76 T 6.27 -T 4.92*

17.00 16.96 17.03

+ 8.30 + 0.69 +- 0.98

statistically

diabetics

that than

onset

mechanisms

the the

in

support

been

or

in

suggest

the

significant

between-group

differences

obtain

+- SD)

+ 3.46 7 3.11 +- 2.04

other

having

influence

pathogenetic

THE

24.84 25.76 24.16

only all

results

data

OF

analysis was performed by the Student’s t test for 0 in the upper index indicate significant differences the same group (p < 0.05 or 0.005, respectively).

I indicates whereas

these

diabetics

(total)

Table

that

Senile

(total)

diabetics,

the

RESULTS

70 - 86 13 6

statistical data. + and the males in

groups.

MAIN

(years) males females

MMSE

of

70

of

and

I

COMPOSITION

in

State

cerebral

at

diabetics

onset shown

metabolism

deterioration.

the

Scale

glucose

This

interact

evaluating

without

has

performance.

cerebral

Mental

aged

years);

summarized

is

of

the

1994)

that

promoting

regulation

induce

al.,

cognitive

Depression

subjects,

senile

4.71

the

Geriatric

to

et

hypoglycemia in

study

using

the

the

and

(Gold the

and

ongoing

influence

glucose,

influence

neuropathies

Our

to

study

hyperglycemia

ses

able

the

from

collected of

so mental

involving

sex-differences

MMSE

males

and

of

the

further

far

do

GDS

scores

of

is

more

group.

It

same

cerebral

indicate A areas

of our to

deeper in

what

aged

no

performance the

the

revealed

development not

deterioration. the

in

sex-comaprisons

cognititve

unpaired against

sta-

these

3

impaired is

hoped

study.

extent

dia-

understanding diabetic

subjects

46 is required. brain; the

that

able

to to

present

of

disease

a good

prevent define

it

diabetes

duration

doubt

on

At

whether

can

metabolic

metabolic better

is

the

difficult

interacts

to

influence balance

complications. relationships

establish

with

aging the can

Further

takes

impairing,

cerebral prevent

between

what in

place and

in to

performance. cognitive

and

extent

There disorders,

longitudinal diabetes

a diabetic

what

studies the

cerebral

is as

are

no it

is

going deteri-

oration.

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