by medical students Al- kindy college of medicine Baghdad, Iraq

1. TREATABLE CAUSES
OF DEMENTIA
Ali Salam
Hussein Ali
Ali Akram
Azhar Sarmad

2. DEMENTIA
IS DEFINED AS AN ACQUIRED
DETERIORATION IN COGNITIVE ABILITIES
THAT IMPAIRS THE SUCCESSFUL
PERFORMANCE OF ACTIVITIES OF DAILY
LIVING.
IT AFFECTS 5% OF THOSE OVER 65 YEARS
OLD AND 20% OF THOSE OVER 85 YEARS OLD.

3. MEMORY IS THE MOST COMMON
COGNITIVE ABILITY LOST WITH
DEMENTIA OTHERS MAY BE
AFFECTED:
-LANGUAGE.
-VISUOSPATIAL ABILITY.
-CALCULATION.
-JUDGMENT.
-PROBLEM SOLVING.

4. NEUROPSYCHIATRIC AND SOCIAL
DEFICITS ALSO ARISE IN MANY
DEMENTIA SYNDROMES, RESULTING
IN:
-DEPRESSION.
-APATHY.
-HALLUCINATION.
-DELUSIONS.
-AGITATION.
-INSOMNIA.
-DISINHIBITION.

5. THE MOST COMMON FORMS
OF DEMENTIA ARE
PROGRESSIVE, BUT SOME
ARE STATIC AND
UNCHANGING OR FLUCTUATE
FROM DAY TO DAY OR EVEN
MINUTE TO MINUTE.

6. CAUSES OF DEMENTIA

7. REVERSIBLE CAUSES:
1-HYPOTHYROIDISM.
2-THIAMINE DEFICIENCY.
3-VITAMIN B12 DEFICIENCY.
4-NORMAL-PRESSURE HYDROCEPHALUS.
5-SUBDURAL HEMATOMA.
6-CHRONIC INFECTION.
7-BRAIN TUMOR.
8-DRUG INTOXICATION.

8. IRREVERSIBLE CAUSES:
1-ALZHEIMER’S
2-FRONTOTEMPORAL DEMENTIA
3-HUNTINGTON’S
4-DEMENTIA WITH LEWY BODIES
5-VASCULAR
6-LEUKOENCEPHALOPATHIES
7-PARKINSON’S

9. PSYCHIATRIC DISORDER:
1-DEPRESSION.
2-SCHIZOPHRENIA.
3-CONVERSION REACTION.

10. ASSOCIATED TREATABLE
CONDITIONS:
1-DEPRESSION.
2-AGITATION.
3-SEIZURES.
4-INSOMNIA.
5-DRUG SIDE EFFECTS.

11. CLINICAL FEATURES
- THE USUAL PRESENTATION IS WITH
A DISTURBANCE OF PERSONALITY OR
MEMORY DYSFUNCTION.
-A CAREFUL HISTORY IS ESSENTIAL
AND IT IS IMPORTANT TO INTERVIEW
BOTH THE PATIENT AND A CLOSE
FAMILY MEMBER.

13. THE TOTAL SCORE IS 30
*ANY SCORE GREATER THAN OR EQUAL TO 24
POINTS INDICATE NORMAL COGNITION
*(19-23) INDICATE MILD COGNITIVE
IMPAIRMENT
*(10-18) INDICATE MODERATE COGNITIVE
IMPAIRMENT
*(LESS THAN 9) INDICATE SEVERE COGNITIVE
IMPAIRMENT.

14. INITIAL INVESTIGATION
IN MOST PATIENTS:
1-IMAGING OF HEAD (COMPUTED
TOMOGRAPHY (CT) AND/OR
MAGNETIC
RESONANCE IMAGING (MRI)).

15. 2-BLOOD TESTS:
-FULL BLOOD COUNT.
-ERYTHROCYTE SEDIMENTATION RATE.
-UREA AND ELECTROLYTES.
-GLUCOSE AND CALCIUM.
-LIVER AND THYROID FUNCTION TESTS.
-VITAMIN B12
-VENEREAL DISEASES RESEARCH
LABORATORY (VDRL) TEST
-ANTINUCLEAR ANTIBODY (ANA) , ANTI-
DSDNA

16. 3-CHEST X-RAY.
4-EEG.
IN SELECTED PATIENTS
-LUMBAR PUNCTURE.
- HIV SEROLOGY.
-BRAIN BIOPSY.

17. 1. Head injury. This refers to brain damage from accidents, such as falls or beating which in
result cause damage of brain cells and can lead to dementia.
2. Normal pressure hydrocephalus
3. Brain tumours.
4. Infections (such as meningitis, hiv, or syphilis).
5. Hormone disorders (i.E. That is, disorders of hormone-secreting and hormone-regulating
organs such as the thyroid gland).
6. Metabolic disorders (i.E. Such as diseases of the liver, pancreas, or kidneys that disrupt the
balances of chemicals in the blood).
7. Nutritional (i.E. Vitamin) deficiencies, drug abuse, or chronic alcoholism
8. Drugs (any drug with anticholinergic activity)
Treatable cause of Dementia

18. Normal pressure hydrocephalus
• Also called Hakim's syndrome.
• Caused by the build-up of cerebrospinal fluid in
ventricles.
• Usually occurs in older adults. The average age of
person with NPH is over age 60.
• Nph is different than other types of hydrocephalus in that
it develops slowly over time.
• Idiopathic 50 %or secondary to conditions that interfere
with CSF absorption, such as meningitis(4.5%) or
subarachnoid hemorrhage (23%) traumatic brain injury
(12.5%).

19. CLASSIC TRIAD
1. GAIT DISTURBANCE
• Is typically the earliest feature
noted and considered to be the
most responsive to treatment
• No classic gait disturbance
• Gait may be wide based,
shuffling, More severely affected
patients have “magnetic gait”
Clinical features

20. 2. Urinary Incontinence
• True incontinence found only in severely affected patients
• Urinary urgency in most patients with NPH due to stretching of periventricular nerve fibers and
loss of detrusor inhibition.
• Bladder sphincter muscle unaffected.
3. DEMENTIA
• Usually mild.
• Dementia usually least responsive of symptoms to intervention.
• Mental status changes may resemble depression.
• Prominent memory loss, decreased attention, Aphasia and agnosia

21. Pathophysiology
• Not completely understood
• It caused by impaired CSF absorption from arachnoid granulations in the subarachnoid space
over the cerebral hemispheres which lead to increase in ventricular volume.
• Clinical symptoms result from distortion of the central portion of the corona radiata by the
distended ventricles.
• The periventricular white matter anatomically includes the sacral motor fibers that innervate
the legs and the bladder, thus explaining the abnormal gait and incontinence.
• Dementia results from distortion of the periventricular limbic system.

22. Diagnosis
1. History
• Insidious onset
• Age over 40
• Symptom duration 3-6 months
• No antecedent event known to cause secondary NPH
• Progressive over time
• No other medical, psychiatric or neurological condition that could cause symptoms.
2. Clinical

23. 3. The CT scan or MRI
4. Lumbar puncture
5. radionuclide cisternogram is a medical imaging study which involves injecting
a radionuclide by lumbar puncture (spinal tap) into a patient's cerebral spinal fluid (CSF) to
determine if there is abnormal CSF flow within the brain and spinal canal
Tap test or external lumbar drainage = (DX) !
Diagnosis

24. Treatment
• Patients with hydrocephalus from meningitis or subarachnoid hemorrhage, recover or
improve after ventriculoatrial, ventriculoperitoneal, or lumboperitoneal shunting.
• In idiopathic NPH, approximately 70% of patients respond to shunting. About 15%
require shunt revision and about 10% experience complications such as subdural or
intracerebral hemorrhage, seizures, or infection.

25. Lumboperitoneal shunt

26. Brain tumor

27. • The dementia associated with brain tumor is characterized by prominent mental slowness,
apathy, impaired concentration, and subtle alterations in personality.
• Depending on the areas of involvement, memory disorder, aphasia, or agnosia may be seen
early.
• Brain tumors ultimately produce headache, seizures, or focal sensorimotor disturbances.
• Meningeal neoplasia, may also produce dementia that is commonly associated with
headache, as well as symptoms and signs of dysfunction at multiple sites in the nervous
system.
• The diagnosis is established by cytologic studies of the CSF.
Brain tumor

28. • Brain tumors produce dementia and related syndromes by a combination of local and
diffuse effects, including edema, compression of adjacent brain structures, increased
intracranial pressure, impairment of cerebral blood flow, and disruption of brain
connectivity.
• Cognitive function in patients with brain tumor can also be impaired by radiotherapy
or chemotherapy.
• The tumors most likely to produce generalized cerebral syndromes are gliomas arising
in the frontal or temporal lobes or the corpus callosum.

29. Is a neurodegenerative disease found in people who have had multiple head injuries.
It is most commonly found in those who have participated in contact sports on a regular
basis.
Chronic traumatic encephalopathy (CTE)

32. • The degeneration caused by a protein called Tau forms clumps that slowly spread
throughout the brain, killing brain cells.
• CTE can only be definitively diagnosed by direct tissue examination after death, including
full and immunohistochemical brain analyses.
• Concussions are non-structural injuries and do not result in brain bleeding, which is why
most concussions cannot be seen on routine neuroimaging tests such as CT or MRI
Diagnosis

33. • CTE is a progressive, degenerative brain disease for which there is no treatment.
• The current approach is to prevent head injury.
• It's also important to stay informed about the latest recommendations for detecting
and managing traumatic brain injury.
Prognosis

34. INFECTIONS
• HIV-ASSOCIATED NEUROCOGNITIVE DISORDERS
• Neurosyphilis

35. HIV-ASSOCIATED
NEUROCOGNITIVE DISORDERS
• (HIV-1) infection of the brain can produce a range of HIV-associated
neurocognitive disorders. These include asymptomatic neurocognitive
impairment (demonstrable only by cognitive testing), minor
neurocognitive disorder (mild to moderate cognitive and functional
impairment) , HIV-associated dementia (moderate to severe cognitive and
functional impairment).
• combination antiretroviral therapy reduce the incidence , but its
prevalence has increased as patients live longer.
• Risk factors include intravenous drug use, female gender, and increased
age.

36. PATHOGENESIS
• HIV-associated dementia results from invasion of the brain by blood-borne
macrophage-tropic retrovirus, which infects macrophages, microglia, and
astrocytes, but not neurons.
• The virus appears to reach the CNS early in the course of systemic HIV-1 infection,
but may remain latent and asymptomatic for years. Alternatively it can produce
transient symptomatic HIV-1 meningitis.
• Proposed mechanisms of pathogenesis include neurotoxic effects of viral proteins,
and cytokines, chemokines and other soluble factors released by inflammatory cells.

37. CLINICAL FINDINGS
• The onset of HIV-associated dementia is usually insidious and is associated with
cognitive, behavioral, and motor deficits.
• These include memory loss, apathy, difficulty with reading and writing, gait
disorder, and tremor.
• Cortical deficits such as impaired executive function and learning and parkinsonian
features have also become common with antiretroviral treatment.
• Examination may show primitive reflexes, hyperreflexia, extensor plantar responses,
and cerebellar ataxia.

38. INVESTIGATION
• There is no definitive laboratory test for HIV-associated
dementia.
• CSF may show mild to moderate elevation of protein ,
modest, usually mononuclear pleocytosis , and oligoclonal
bands.
• MRI shows cortical and subcortical atrophy with diffuse
signal abnormalities in subcortical white matter and is
useful for excluding other HIV-related neuropathologic
processes, such as opportunistic infection.
increased signal intensity (arrows)
in subcortical white matter.

39. TREATMENT
• Patients with HIV-associated cognitive disorders should receive combination antiretroviral
therapy.

40. PROGNOSIS
• The course may be relatively static, steadily progressive, or acutely
exacerbated by concurrent disease.
• With combination antiretroviral treatment, median survival has been
extended from a few months to several years

41. NEUROSYPHILIS
• Syphilis is caused by Treponema pallidum transmitted
by sexual contact, which results in infection in
approximately one-third of encounters with infected
individuals.
• Dementia from neurosyphilis (general paresis) was
common in the prepenicillin era but is now rare.

42. CLINICAL FINDINGS
• Primary syphilis = (chancres) that usually appear within 1 month of exposure.
• Hematogenous spread of T. pallidum produces symptoms and signs of secondary
syphilis, within 1 to 6 months.
• Neurologic symptoms are uncommon. Meningeal syphilis, the earliest form of
symptomatic neurosyphilis, occurs 2 to 12 months after primary infection, and is
associated with headache, stiff neck, nausea and vomiting, and cranial nerve (especially
II, VII, or VIII) involvement. Meningovascular syphilis is seen 4 to 7 years into the
course of the disease and usually presents with transient ischemic attacks or stroke

43. CLINICAL FINDINGS
• Late (parenchymatous) neurosyphilis produces the syndromes of general paresis and
tabes dorsalis, which can occur separately or together (taboparesis); either one can occur
in combination with optic atrophy. General paresis is a chronic meningoencephalitis
caused by active spirochetal infection. Onset is with gradual memory loss or altered
affect, personality, or behavior.
• This is followed by global intellectual deterioration with grandiosity, depression,
psychosis, and focal weakness. Terminal features include incontinence, seizures, or
strokes. Neurologic examination may show tremor of the face and tongue, paucity of
facial expression, dysarthria, and pyramidal signs.

44. SIGNS AND SYMPTOMS OF TABES
DORSALIS

45. INVESTIGATION
• Treponemal serologic blood tests :
A. (fluorescent treponemal antibody absorbed) [FTA-ABS]
B. microhemagglutination-Treponema pallidum [MHATP])
• but non-treponemal blood tests (Venereal Disease Research Laboratory [VDRL] or rapid plasma
reagin [RPR]) can be negative; therefore, a treponemal blood test should be obtained in all
suspected cases.
• lumbar puncture (confirm DX ).

46. TREATMENT
• Treatment is with aqueous penicillin G I.V every 4 hours for 10 to 14
days.
• For penicillin-allergic patients, ceftriaxone 2 g I.V daily for 14 days
or doxycycline 200 mg orally twice daily for 21 to 28 days can be
substituted.
• The CSF should be examined every 6 months until all findings are
normal.
• Another course of therapy must be given if the CSF cell count or
protein remains elevated.

47. PROGNOSIS
•General paresis may improve or stabilize after treatment,
but in some cases it continues to worsen. Patients with
persistently reactive CSF serologic tests but no pleocytosis
are unlikely to respond to penicillin therapy but are
usuallytreatednevertheless.

48. PROGRESSIVE MULTIFOCAL
LEUKOENCEPHALOPATHY (PML)
• Progressive multifocal leukoencephalopathy (PML) results from reactivation of
JC virus infection, in immunosuppressed patients. These include individuals
with lymphoma, leukemia, or HIV infection, and those treated for multiple
sclerosis or Crohn disease with natalizumab or for psoriasis with efalizumab. The
disease targets oligodendrocytes, leading to diffuse and patchy demyelination
of the cerebral hemispheres, brainstem, and cerebellum. The course is typically
subacute and progressive, leading to death in approximately 50% of patients
within 3 to 6 months, although mortality is lower (approximately 20%) in
patients on natalizumab. PML associated with natalizumab or efalizumab does
not occur until years after treatment.

49. IMMUNOHISTOCHEMICAL
DETECTION OF JC VIRUS PROTEIN
(STAINED BROWN) IN A BRAIN
BIOPSY (GLIAL CELLS
DEMONSTRATING PROGRESSIVE
MULTIFOCAL LEUKOENCEPHALOPATH
(PML))

50. SIGNS AND SYMPTOMS
•Fever and systemic symptoms are absent.
Dementia and focal cortical dysfunction are
prominent. Signs include hemiparesis, visual
deficits, aphasia, dysarthria, and sensory
impairment. Ataxia and headache are
uncommon, and seizures do not occur.

51. INVESTIGATIONS
A. CSF is usually normal but may show a mild increase in pressure, white cell
count, or protein.
B. The CT scan or MRI shows multifocal white matter abnormalities.
C. When the diagnosis is in doubt, it can be established by brain biopsy.

52. AXIAL FLAIR MRI IN
PROGRESSIVE
MULTIFOCAL
LEUKOENCEPHALOPHY,
SHOWING ABNORMALLY
HIGH SIGNAL INTENSITY
IN WHITE MATTER OF
THE RIGHT PARIETAL
AND OCCIPITAL LOBES.

53. TREATMENT
Treatment of PML is with combination
antiretroviral therapy for patients with HIV
infection and discontinuation of the drug and
plasma exchange for patients receiving
natalizumab.

54. ALCOHOLIC DEMENTIA
• Alcoholic dementia caused by direct toxic effects of ethanol on the brain has been
proposed to occur, but no distinctive abnormalities have been identified in the
brains of demented alcoholics. Dementia in alcoholics is more likely the result
of one of the metabolic and traumatic disorders, or misdiagnosis of Korsakoff
syndrome

55. • Treatment with thiamine should be started immediately without waiting
for the results.
• Every patient with alcohol dependence should be advised to strive for total
abstinence. Lifestyle changes in form of exercise and healthy diet is also
important. In cases with cognitive impairment, memory training
techniques along with social support is required.

56. HYPOTHYROIDISM
• Hypothyroidism (myxedema), which is cause of acute confusional states, can also
produce a reversible dementia or chronic organic psychosis.. Psychiatric manifestations are
typically prominent and include depression, paranoia, visual and auditory
hallucinations, mania, and suicidal behavior.

57. TREATMENT
• This involves intravenous administration of levothyroxine (400 μg, then 50-100 μg
daily), with hydrocortisone (100 mg, then 25-50 mg every 8 hours) for associated
adrenal insufficiency.