IPHREHAB : CEREBRAL ISCHEMIA AND INFARCTION

IPHREHAB :

 CEREBRAL ISCHEMIA AND INFARCTION


Cerebral ischaemia and infarction
Anatomy and pathology
The principal pathological process under consideration here is the occlusion of arteries supplying the brain. The two internal carotid arteries and the basilar artery form the Circle of Willis at the base of the brain, which acts as an efficient anatomotic device in the event of occlusion of arteries proximal to it.

CIRCLE OF WILLIS

Anatomy and pathology

VERTEBRAL ARTERY

Occlusion leads to sudden severe ischaemia in the area of brain tissue supplied by the occluded artery, and recovery depends upon rapid lysis or fragmentation of the occluding material: Reversal of neurological function within minutes or hours gives rise  to the clinical picture of a transient ischaemic attack.

When the neurological deficit lasts longer than 24 hours, it may be called a reversible ischaemic neurological deficit ( RIND ) if it recovers completely in a few days, or a completed stroke if there is a persistent deficit. Sometimes recovery is very slow and incomplete.

Neurological symptoms and signs  

The loss of function that the patient notices, and which may be apparent on examination, entirely depends on the area of brain tissue involved in the ischaemic process.      

 Neurological symptoms and signs

BASIC

The following suggest middle cerebral territory:

Dysphasia; Dyslexia, dysgraphia, dyscalculia; Loss of use of contralateral face and arm; Loss of feeling in contralateral face and arm.

• The following suggests anterior cerebral territory:

Loss of use and/ or feeling in the contralateral leg.

• The following suggests posterior cerebral territory:

Development of a contralateral homonymous hemianopia.

Neurological symptoms and signs

The following suggests a deep-seated lesion affecting the internal capsule which is supplied by small perforating branches of the middle and posterior cerebral arteries close to their origins: Complete loss of motor and sensory function throughout the whole of the contralateral side of the body with a homonymous hemianopia.

Neurological symptoms and signs

The following suggests ophthalmic artery territory (the ophthalmic artery arises from the internal carotid artery just below the Circle of Willis): Monocular loss of vision.

Neurological symptoms and signs

The following suggest vertebro-basilar territory: double vision( 3,4,6);

facial numbness(5);

facial weakness(7);

vertigo (8);

dysphagia (9, 10);

dysarthria ( 9, 10, 12);

ataxia; drop attacks;

motor or sensory loss in both arms or legs.

IPHREHAB : OBESITY..REGULTAION

IPHREHAB

OBESITY.

PHYSIOLOGY

Body weight is regulated

• Endocrinal Component
• Neural components 

Small imbalances between energy intake and expenditure will ultimately have large effects on body weight. 

For example, a 0.3% positive imbalance over 30 years would result in a 9-kg weight. gain

NORMAL REGULATION

There is autoregulation weight

Weight loss increases appetite and energy expenditure falls 

With overfeeding, appetite falls and energy expenditure increases. 

This latter compensatory mechanism frequently fails in OBESE PERSONS, permitting obesity to develop when food is abundant and physical activity is limited. 

REGULATION-LEPTIN

Leptin is hormone which is a major regulator of these adaptative responses

It is the adipocyte-derived hormone

 Leptin, acts through brain circuits (predominantly in the hypothalamus) to influence appetite, energy expenditure, and neuroendocrine function

APPETITE CENTRE

Appetite centre is in the the hypothalamus Signals affecting on the hypothalamic are neural, hormonal , and metabolic. 

Vagal inputs are particularly important, bringing information from gut distention. 

Hormonal signals include leptin, insulin, cortisol, and cholecystokinin, which signals to the brain through the vagus nerve. 

Metabolites as glucose also  influence appetite.  Hypoglycemia  induces  hunger

The hormonal, metabolic, and neural signals  can act by influencing the expression and release of various hypothalamic peptides [neuropeptide} 

Psychological and cultural factors also play a role in the final expression of appetite. Apart from rare syndromes involving leptin, its receptor, and the melanocortin system the defects in this complex appetite control network that account for common causes of obesity are not well understood.