T2 Weighted MRI of a Man with Dementia

Sunday, January 3, 2010
This is an Axial T2 Weighted MRI of the brain of 61 year old male patient who has been having severe cognitive impaitement over last 8 months.And His relatives has noticed that he was having mood disturbances personality changes also.Comment on this MRI?

ANSWER -T2 weighted MRI of the Brain which shows atrophic changes in the Temporal Lobes (Alzheimer’s disease)

According to the short Hx given here this patient was having some sort of chronic dementia.Dementia may be defined as a global deterioration in intellectual function, behaviour and personality in the presence of normal consciousness and perception.Many causes of dementia are irreversible

The most common causes for the dementia are
Primary dementia disorders -:
Alzheimer’s disease (60-80%)
Vascular dementia (10-20%)
Dementia with Lewy bodies
Parkinson’s disease dementia

Potentially reversible dementia disorders
Depressive pseudo dementia
SOL eg: subfrontal meningioma , chronic SDH
Hydrocephalus eg: NPH(normal pressure hydrocephalus)
Deficiency stateseg: Vit B12
Endocrine and metabolic causeseg: Hypothyroidism, Recurrent Hypoglycaemia, Uraemia, Hepatic Encephalopathy
InfectionsHIV,Syphilis,Mad cow disease
Vasculitis eg: SLE
Alcohol related dementia

Alzheimer Disease

The most common neurodegenerative disease.It is the Commenest cause of dementia.Aetiology unknown
Risk factors:
  1. Age
  2. Family history
  3. Genetic (Apo E polymorphism ε4 gene)
  4. Vascular risk factors and the metabolic syndrome
  5. Female gender

Alzheimer's disease is principally characterised by neurofibrillary tangles and senile plaques.Neurofibrillary tangles are found particularly in pyramidal cells of the association neocortex, in the hippocampus, and in certain subcortical nuclei which send projections to the cerebral cortex.
Senile plaques consist of dystrophic axons and dendrites clustered around an amyloid core.
Amyloid is composed of beta amyloid protein which is a proteolytic fragment of a larger membrane-spanning protein called beta-amyloid precursor protein.

AD Clinical Syndrome
•Insidious onset & slowly progressive
•Impaired recent memory – most prominent feature early in the disease.
•Deficit in new learning – forget names, phone numbers, important dates)
•Visuo-spatial disorientation, misplacement of items, difficulty in navigating a familiar terrain.
•Functional loss: financial affairs, inability with tasks in one’s job and home.

Later AD
•Progression of disorders of memory, thinking orientation and behaviour.
•Recent information are instantly forgotten.
•Language dysfunction: word finding difficulties,reduced vocabulary and spontaneous speech.
•Inability to recognise friends, family and own home.
•Progressive difficulty with complex multistep motor activities.(Apraxia)
Dependant on others for ADL

Terminal AD
•Negligible memory for events, conversation and family members.
•Patient may be virtually mute.
•Need 24 hr supervision for ADL.
•May become aggressive, experience depression, anxiety and fear.
•Extra pyramidal signs.
•Death 7-12 yrs from the diagnosis.

Mental State Examination (MMSE - 30 points) can be used to classify the severity of cognitive impairment in Alzheimer's disease
  • mild Alzheimer's disease: MMSE 21 to 26
  • moderate Alzheimer's disease: MMSE 10 to 20
  • moderately severe Alzheimer's disease: MMSE 10 to 14
  • severe Alzheimer's disease: MMSE less than 10
The diagnosis requires confirmation at post-mortem,
although in practise it is made on clinical grounds.

Treatment of AD
  1. Supportive therapy
  2. Cholin Esterase Inhibitors (ChEIs)
  3. Donepezil, Rivastigmine, Galantamine
  4. Side effects(20%) - nausea, vomitting, diarrhoea



  1. shameel Says:
  2. Generalised Brain atropy and flattening of gyri..
    Alzheimer's disease..

  3. Anonymous Says:
  4. flattening of guyri and sulsi is seen in MRI can be due to lewy body syndrome or prion disease which can ultimately lead to Alzheimers disease a major cause of Dementia

  5. My dad has this and it is really sad but annoying at times as he never remembers anything i tell him .


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