2. Dementia
“Dementia” refers to loss of memory with
impairment of any other cognitive function sufcient
to interfere with social or occupational functioning.
Cognitive function is measured by various mental
functions, including memory, concentration,
language, praxis, visuospatial functioning, and
executive functions.
3. There are more than 100 identifiable causes of
dementia in the elderly.
1. Reversible causes include hypothyroidism, vitamin
B12 deficiency, hepatic or uremic encephalopathy,
CNS vasculitis, syphilis, brain abscess, brain tumor
(primary or metastatic), medications (especially
anticholinergics), obstructive sleep apnea, central
sleep apnea, trauma, subdural hematoma, normal
pressure hydrocephalus (NPH), and depression.
4. 2. Irreversible causes include progressive
multifocal leukoencephalopathy, Alzheimer
disease (60–80% of all cases), dementia with
Lewy bodies, frontotemporal degeneration,
vascular dementia including multi-infarct
dementia .
5. Old age remains to be the most important risk
factor for dementia.
Young onset dementia is considered when the
onset is before the age of 65.
Other risk factors for dementia include family
history, history of cardiovascular or
cerebrovascular disease, diabetes, obesity,
alcohol, anticholinergic medications
6. The prevalence of dementia is
1–5% at ages 65–69, and
rising to 45% by age 100.
Only 5% of Alzheimer disease is
inherited.
7. Clinical Presentation
The most common cause of dementia is
Alzheimer disease.
Typically, patients will present with problems in
memory and visuospatial abilities that generally
occur early in the course of the disease.
Social graces can be retained despite signifcant
loss of cognitive decline.
Hallucinations and personality changes typically
occur late in the course of the disease.
8. Mild cognitive impairment refers to memory
loss without dysfunction of other cognitive
domains.
These patients have a higher risk of
developing Alzheimer disease later in life but
do not have Alzheimer disease.
The rate of progression is 15–20% per year.
9. Patients with frontotemporal dementias such as Pick
diseasell typically present with personality changes
early in the course of their disease, with relative
sparing of their visuospatial function.
Social, interpersonal, and emotional abnormalities
precede memory impairment.
Frontotemporal dementia is ofen noted primarily by
the family because the patient lacks
insight into their condition.
There is no proven therapy for this condition.
10. • Dementia secondary to Parkinson disease
should be accompanied by clinical fndings
consistent with that disease.
• Recurrent visual hallucinations are also
characteristic.
11. • Vascular dementia is divided into multi-infarct
dementia, which typically has a stepwise
progression associated with discrete
cerebrovascular events, and Binswanger
disease, involving the subcortical white
matter, which presents with a slowly
progressive course.
12. Diagnosis
All patients with cognitive impairment should be
assessed with a Mini Mental Status Examination
(MMSE) to identify the areas of cognitive impairment
Initially, the workup should focus on ruling out
reversible causes of the dementia.
If a reversible cause is identifed, it should be treated,
with the hope that cognitive function can be
recovered.
Laboratory studies should include a complete blood
count (CBC), electrolytes, calcium, creatinine,
liver function studies, glucose, thyroid-stimulating
hormone (TSH), vitamin B12, RPR,
13. • Brain imaging is most useful for patients who
have a focal neurologic exam, seizures, gait
abnormalities, and an acute or subacute onset
of their symptoms.
14. Treatment.
• Treatment of dementia revolves around
insuring that the family and the patient
have the proper medical and emotional
support to cope with the disease.
• Caregivers are at an increased risk for
depression and anxiety.
• Their concerns and frustrations should be
addressed at frequent intervals.
15. Alzheimer disease (AD) is an acquired disorder
of cognitive and behavioral impairment that
markedly interferes with social and
occupational functioning.
It is an incurable disease with a long and
progressive course.
16. • Alzheimer disease is, by defnition, the loss of
memory as well as other cognitive disturbances,
such as aphasia, agnosia (the failure to identify
entities despite intact sensory function),
apraxia, or the loss of the ability to make plans
and execute them. There is no single diagnostic
test for Alzheimer disease
17. . In AD, plaques develop in the hippocampus, a
structure deep in the brain that helps to encode
memories, and in other areas of the cerebral cortex
that are used in thinking and making decisions.
Whether plaques themselves cause AD or whether
they are a by-product of the AD process is still
unknown.
Currently, an autopsy or brain biopsy is the only way to
make a definitive diagnosis of AD.
In clinical practice, the diagnosis is usually made on the
basis of the history and findings on Mental Status
Examination
18. Alzheimer’s disease usually has an insidious onset,
leading to death within 8–10 years after symptoms
are first recognized.
Estimates of its prevalence range from 5% at age 65
to 40% by age 90.
19. Risk factors include a history of head injury,
Down syndrome, low educational and
occupational level, and having a first-degree
relative with Alzheimer’s disease.
In fact, up to 50% of the first-degree relatives
of persons with Alzheimer’s disease are
affected with the disorder by age 90 years.
20. Symptoms worsen progressively, eventually
resulting in near collapse of cognitive functioning.
Physical findings are generally absent, or they are
present only in later stages: hyperactive deep
tendon reflexes, Babinski’s sign, and frontal lobe
release signs.
The presence of illusions, hallucinations, or
delusions is associated with accelerated cognitive
deterioration.
21. Cortical atrophy and enlarged cerebral ventricles are
typically seen on CT or MRI scans.
Alzheimer’s disease has been associated with a
reduction in CSF amyloid levels compared with those in
healthy subjects, which is thought to be due to
sequestration of the amyloid within the neuronal
plaques.
Conversely, tau protein is elevated in the CSF of
Alzheimer’s patients compared to controls.
22. • Raising the level of acetylcholine in CSF
benefts patients with Alzheimer diseas,
23. Seizure : paroxysmal event due to abnormal ,
excessive, hypersynchronous, discharges from
an aggregates of CNS neurons.
it is an abnormal electriical discharge in the
brain.
• 5-10% of the population will have at least one
seizure during their lifetime
• Common : early childhood & late adulthood
Epilepsy: recurrent seizure( 2 or more
unprovoked seizures
24. …cont
1. Partial seizures
a. Simple partial seizure(with motor , sensory, autonomic or
psychic signs)
b. Complex partial seizure
c. Partial seizure with secondary generalization
2. Primary generalized seizures
a. Absence (petit mal)
b. Tonic- clonic ( grand mal)
c. Tonic
d. Atonic
e. Myoclonic
3. unclassified: neonatal seizures & infantile spasms
25. Partial seizures
Partial :often associated with structural
abnormalities of the brain
Simple partial seizure:
- Local EEG abnormality
- Additional features:
*Epilepsia partialis continua(hours to days)
- Sensory : eg visual hallucination
- Autonomic: eg sweating
- Psychic: eg fear
26. Complex partial seizures
• Focal seizure with impairment to respond to
visual or verbal command
• Begins with aura( i.e. simple partial seizure)
• Amnestic (ictal phase)
• Usually accompanied by automatism eg
chewing, swallowing
• Most complex partial seizures arise from the
temporal lobe
27. Generalized tonic-clonic seizure(GTCS)
The most common seizure type resulting from
metabolic derangements.
• Usually begins abruptly without warning
- Tonic contraction : loud cry
- impaired respiration
- Increased secretion
- Cyanosis
- Biting of tongue
- Incontinence
- Postictal confusion ,headache ,fatigue , muscle ache
29. Evaluation of the patient
Diagnosis has 3 objectives
1. Establishing whether the reported episode
was a seizure
2. Determine the cause
identify – risk factors
- precipitating events
3. Decide whether anticonvulsant is required
30. …cont
• History
- interview witness
- auras
- Head injury/ C NS infection/stroke
- Precipitating event:stress,sleep deprivation
- Family history
• P/E
- Usually normal ,Signs of infection
- Chronic renal failure ,chronic liver disease,Cardiovascular abn.
- Complete neurological exam
32. Treatment
• Multimodal
• Education
• Individualized
A. Treatment of underlying condition e.g.
hypoglycemia( need no anticonvulsant drug)
B. Avoidance of precipitating factors
C. Antiepileptic drug therapy(AED)
- mainstay
- goal = no seizure
- needs classification of seizure
