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A 60 year old man with Progressive Dementia and sillly behavior

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Information about A 60 year old man with Progressive Dementia and sillly behavior

Published on May 3, 2007

Author: NeurologyGuru

Source: slideshare.net

Description

A 60 year old man with Progressive Dementia and “silly behavior”:- Case Discussion
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Progressive Dementia and “silly behavior” Submitted to AskTheNeurologist.Com in 2007 Author Anon.

60 year old man R handed Married + 2 children Admitted electively with complaints of cognitive decline and gait difficulty for the past 2 ½ years

60 year old man

R handed

Married + 2 children

Admitted electively with complaints of cognitive decline and gait difficulty for the past 2 ½ years

History (collateral) 2 ½ years prior to admission patient had a RTA ( unclear how) without head injury From that point family became aware of cognitive changes: - Apathy Memory disturbance

2 ½ years prior to admission patient had a RTA ( unclear how) without head injury

From that point family became aware of cognitive changes:

- Apathy

Memory disturbance

History 2 Over following months cognitive complaints exacerbated Unable to find way around familiar places Urinary incontinence Began to develop behavioural changes especially “jokiness” with inappropriate comments

Over following months cognitive complaints exacerbated

Unable to find way around familiar places

Urinary incontinence

Began to develop behavioural changes especially “jokiness” with inappropriate comments

History 3 About 8 months prior to admission family noticed gait disturbance and other movements becoming difficult - Standing from sitting - Turning over in bed In addition cognitive aspects continued to deteriorate, 6 months ago had to close shop Kept returning to shop and believed someone was trying to steal from him Overeating and weight gain Referred for elective admission

About 8 months prior to admission family noticed gait disturbance and other movements becoming difficult

- Standing from sitting

- Turning over in bed

In addition cognitive aspects continued to deteriorate, 6 months ago had to close shop

Kept returning to shop and believed someone was trying to steal from him

Overeating and weight gain

Referred for elective admission

History 4 Patient / family deny: Step-wise deteriorations Myoclonus Language disorder Headache Falls

Patient / family deny:

Step-wise deteriorations

Myoclonus

Language disorder

Headache

Falls

Past history Hyperlipidemia Denies: Diabetes Smoking HTN IHD Alcoholism Treated with aspirin only

Hyperlipidemia

Denies:

Diabetes

Smoking

HTN

IHD

Alcoholism

Treated with aspirin only

Examination General examination unremarkable Fully conscious Cranial nerves: Mild facial asymmetry ( R side weak) Otherwise intact, no gaze or visual disturbace

General examination unremarkable

Fully conscious

Cranial nerves:

Mild facial asymmetry ( R side weak)

Otherwise intact, no gaze or visual disturbace

Examination 2 Motor: Tone increased on R side (“ paratonia”) Power 5/5 x 4 Reflexes increased, more on right Bilateral pyramidal signs

Motor:

Tone increased on R side (“ paratonia”)

Power 5/5 x 4

Reflexes increased, more on right

Bilateral pyramidal signs

Examination 3 Sensory examination unremarkable No cerebellar signs Romberg –ve Gait intact Movement apraxia Difficulty changing postion without any weakness

Sensory examination unremarkable

No cerebellar signs

Romberg –ve

Gait intact

Movement apraxia

Difficulty changing postion without any weakness

Cognitive 1 MMSE 16 / 30 Lack of orientation in time Partial lack of orientation in space -Stimulus-bound responses - Disturbance of concentration Disturbance of STM Occasional “ silly responses”

MMSE 16 / 30

Lack of orientation in time

Partial lack of orientation in space

-Stimulus-bound responses

- Disturbance of concentration

Disturbance of STM

Occasional “ silly responses”

Cognitive 2 Occipital Mild visual object agnosia (L OT) No Field defects Other defects of higher visual function

Occipital

Mild visual object agnosia (L OT)

No

Field defects

Other defects of higher visual function

Cognitive 3 Parietal Topographagnosia ( R PO) Ideomotor apaxia (L) Constructional apraxia (R) NO: Neglect Astereognosis / agraphaesthesia

Parietal

Topographagnosia ( R PO)

Ideomotor apaxia (L)

Constructional apraxia (R)

NO:

Neglect

Astereognosis / agraphaesthesia

Cognitive 4 Temporal Semantic paraphasias Disturbed time perception

Temporal

Semantic paraphasias

Disturbed time perception

Frontal: Witzelsucht Tactlessness Abulia Lack of attention Stimulus-bound Concrete thinking Difficulty with abstraction Perseveration Cognitive 5 Release signs PMR bilaterally Pout No grasp ( reverse grasping)

Frontal:

Witzelsucht

Tactlessness

Abulia

Lack of attention

Stimulus-bound

Concrete thinking

Difficulty with abstraction

Perseveration

Release signs

PMR bilaterally

Pout

No grasp

( reverse grasping)

Blood work-up prior to admission FBC normal Bioch normal ESR 38 TSH 1.29 ( antithyroglobulin negative) B1 / B12 / Folate normal ANA / ENA /VDRL all negative

FBC normal

Bioch normal

ESR 38

TSH 1.29 ( antithyroglobulin negative)

B1 / B12 / Folate normal

ANA / ENA /VDRL all negative

Investigations FBC normal Bioch normal ESR 68 TSH 1.79 ( antithyroglobulin negative) B12 / Folate normal LP: - TP 597 - no cells EEG normal

FBC normal

Bioch normal

ESR 68

TSH 1.79 ( antithyroglobulin negative)

B12 / Folate normal

LP: - TP 597

- no cells

EEG normal

Brain MRI

 

 

Paper Summary FTD is a clinical syndrome Behavioral or Language presentation ( or combination ) Pathologically heterogeneous

FTD is a clinical syndrome

Behavioral or Language presentation

( or combination )

Pathologically heterogeneous

 

 

 

 

 

 

 

Structural Imaging Magnetic resonance imaging (MRI) scans indicate that both primary progressive aphasia (PPA) and FTD patients show frontotemporal atrophy In PPA patients the focus of atrophy is in the left temporal lobe Focus of atrophy is mainly in R frontal lobe in “FTD” patients In AD , the mesial temporal lobes are specifically atrophic in

Structural Imaging

Magnetic resonance imaging (MRI) scans indicate that both primary progressive aphasia (PPA) and FTD patients show frontotemporal atrophy

In PPA patients the focus of atrophy is in the left temporal lobe

Focus of atrophy is mainly in R frontal lobe in “FTD” patients

In AD , the mesial temporal lobes are specifically atrophic in

 

 

Paper Summary Overlap between FTD, PSP, CBD Clinical FTD Clinical CBD Pathologically FTD Pathologically CBD

Overlap between FTD, PSP, CBD

Clinical FTD Clinical CBD

Pathologically FTD Pathologically CBD

Clinicopathological Heterogeneity In 32 autopsied cases of the CBS pathology: CBD 18 Alzheimer’s disease 3 Pick’s disease 2 PSP 6 Dementia lacking distinctive histology 2 Creutzfeldt–Jakob disease 3

Clinicopathological Heterogeneity

In 32 autopsied cases of the CBS pathology:

CBD 18

Alzheimer’s disease 3

Pick’s disease 2

PSP 6

Dementia lacking distinctive histology 2

Creutzfeldt–Jakob disease 3

MRI Findings in “ corticobasal syndrome” Asymmetrical cortical atrophy, especially frontoparietal Asymmetrical atrophy in the basal ganglia, lateral ventricles, and cerebral peduncles Atrophy of the middle or posterior segment of the corpus callosum Signal changes in the putamen Hyperintense subcortical signal changes in motor and somatosensory cortex

Asymmetrical cortical atrophy, especially frontoparietal

Asymmetrical atrophy in the basal ganglia, lateral

ventricles, and cerebral peduncles

Atrophy of the middle or posterior segment of the corpus callosum

Signal changes in the putamen

Hyperintense subcortical signal changes in motor and somatosensory cortex

 

Conclusions An increased plasma homocysteine level is a strong, independent risk factor for the development of dementia and Alzheimer’s disease. (N Engl J Med 2002;346:476-83.) Above independent of any association with vascular dementia Out of 111 subjects: - AD 78 - VD 11 - “ non AD degenerative dementias” 11 - other 6

 

 

Case report 62 year old with 3 year history of - apathy - confusion - paranoid delusions , loss of social graces - no localisin g signs - frontal release signs - cognitive syndrome - attention ( + STM) - perseveration - preserved language

62 year old with 3 year history of

- apathy

- confusion

- paranoid delusions , loss of social graces

- no localisin g signs

- frontal release signs

- cognitive syndrome - attention ( + STM)

- perseveration

- preserved language

CADASIL MRI

CADASIL skin biopsy

 

 

Summary FTD (clinically, cortical atrophy, w.matter ) CBS (asymmetric rigidity, parietal signs, overlap with FTD, frequent w. matter signs, bulk of syndrome frontal ) Vascular aetiologies should be excluded - “ stroke in the young” esp. homocysteine - ? Skin biopsy - ? Angio If above all negative consider brain biopsy Classical “ white matter diseases ” very unlikely due to extensive cortical involvement both clinically and radiologically

FTD (clinically, cortical atrophy, w.matter )

CBS (asymmetric rigidity, parietal signs, overlap with FTD, frequent w. matter signs, bulk of syndrome frontal )

Vascular aetiologies should be excluded

- “ stroke in the young” esp. homocysteine

- ? Skin biopsy

- ? Angio

If above all negative consider brain biopsy

Classical “ white matter diseases ” very unlikely due to extensive cortical involvement both clinically and radiologically

Submitted to AskTheNeurologist.Com in 2007 Author Anon.

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