2.  The rehabilitation goal for every patient with temporary or permanent cognitive impairment is to promote maximal involvement in self care and meaningful life activities.  The patients with cognitive limitations presents a unique set of needs because hands –on care and touch, rather than speech, eventually become the key tools for communication.

3.  Delirium:  A decline in the level of cognitive function combined with drowsiness or agitation

4.  A global decline in cognitive abilities in a person who is awake and aware of surroundings. The decline from previous status affects several kinds of cognitive tasks.  Alzhemer’s disease is a diagnosis that is made after ruling out the major cause of cognitive impairment such as depression, cerebral infarct, Thyroid dysfunction, Normal pressure hydrocephalus tuberculosis,metal poisoning and Parkinsonism

5.  AD is the most common cause of dementia in people AD 65 years and older 65 older.  Affects 10% of people over the age of 65 and 50% of Affects people over the age of 85people 85  Dr. Murad said the aged, especially those above 60, constitute an estimated 5 to 10 percent of the Kingdom’s population of 22million.  The prevalence of AD IN SAUDI ARABIA 379,35 (25,795,938 2- POPULATION ESTIMATE USED)

6.  Alzheimer’s disease is a brain disorder named for German physician known as Alois Alzheimer, who first described it in 1906.  Scientists have learned a great deal about Alzheimer’s disease in the century since Dr. Alzheimer first drew attention to it. Today we know that Alzheimer’s:  Is a progressive and fatal brain disease.  As many as 26 million people around the world are living with Alzheimer’s disease.  Alzheimer's destroys brain cells, causing problems with memory, thinking and behaviour.  severe enough to affect work, lifelong hobbies or social life.  Alzheimer’s gets worse over time, and it is fatal.  Today it is the sixth-leading cause of death in the world.

7.  The brain has 100 billion nerve cells (neurons). Each nerve cell communicates with many others to form networks.  In Alzheimer’s disease, as in other types of dementia, increasing numbers of brain cells deteriorate and die. Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells.  Plaques build up between nerve cells. They contain deposits of a protein fragment called beta-amyloid.  Tangles are twisted fibers of another protein called tau. Tangles form inside dying cells.  Scientists are not absolutely sure what role plaques and tangles play in Alzheimer’s disease. Most experts believe they somehow block communication among nerve cells and disrupt activities that cells need to survive.

8.  There are 3 consistent neuro pathological hallmarks:  Amyloid-rich senile plaques  Neuro fibrillary tangles  Neuronal degeneration  These changes eventually lead to clinical symptoms, but they begin years before the onset of symptoms Pathology of AD:

10.  Acetylcholine (ACh) is an important neurotransmitter in areas of the brain involved in memory formation  Loss of Ach activity correlates with the severity of AD

11.  Recent memory loss affecting skill in performing job or tasks.  Difficulty performing familiar tasks  Problems with language  Disorientation in terms of time and place  Poor or decreased judgment  Problems with abstract thinking  Misplacing things  Changes in mood or behavior  Changes in personality  Loss of initiative.

12.  Low energy,  emotional liability,  slow reactions,  picking up new information slowly,  less initiative, greater reluctance to try new things.  sticking to familiar activities,  heightened anxiety, difficulty in finance, remembering names, way to familiar places.

13.  Trouble recognizing familiar people  Difficulty in making decisions  Little speech with content  Writing illegibly  Sundown syndrome: experiencing late afternoon restlessness  Difficulty in motor perception and coordination

14.  Apathetic and remote  Unable to recognize self & family  Poor memory  Losing orientation  Becoming incontinent  Inability to communicate  Seizures  Difficulty in ambulation.

15.  Ask both the patient & a reliable informant about the patient’s:  Current condition  Medical history  Current medications & medication history  Patterns of alcohol use or abuse  Living arrangements

16.  Examine:  Neurologic status  Mental status  Functional status  Include:  Quantified screens for cognition › –e.g., Folstein’s MMSE, Mini-Cog  Neuro psychologic testing

17.  Onset occurs at age < 65 years  Symptoms have occurred for < 2 years  Neurologic signs are asymmetric  Clinical picture suggests normal-pressure hydrocephalus  Consider:  Non contrast computed topography head scan  Magnetic resonance imaging  Positron emission tomography

18.  Has no current cure.  But treatment for symptoms, combined with the right services and support, can make life better for the millions of people living with Alzheimer’s.  There is an accelerating worldwide effort under way to find better ways to treat the disease, delay its onset, or prevent it from developing

19.  Primary goals:  To enhance quality of life & maximize functional performance by improving cognition, mood, and behaviour.  Cognitive enhancement  Individual and group therapy  Regular appointments  Communication with family, caregivers  Environmental modification  Attention to safety

20.  Cholinesterase inhibitors: donepezil, rivastigmine, galantamine  Other cognitive enhancers: oestrogen, NSAIDs, ginkgo biloba, vitamin E  Antidepressants  Antipsychotics

21.  Key strategy:  is to build on patient’s intact skills,  to explore new possibilities for communications and  to create a sense of safety and enjoyment that includes modified ADL tasks for the patient.  Guided touch or hands on facilitation can be a strategy to enhance communication, relaxation, balance, coordination, and self determination.