2. 1) DELIRIUM , DEMENTIA
2) HEADACHE
Neurology
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Dr.
Rami
Abo
Ali
2
3. DELIRIUM
Definition:
Delirium is a disorder of brain function affecting
behavior and causing impaired attention and
cognition, altered sleep–wake cycles, and altered
states of arousal.
It is often acute, reversible, and secondary to a
medical or neurologic disorder.
Etiology :
Generalized or focal causes of cerebral
dysfunction are potential causes of delirium 3
Neurology
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Dr.
Rami
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4. DELIRIUM
Generalized brain dysfunction Causes include the
following:
1) Drugs :including anticholinergics , antiparkinsonians ,
analgesics, cimetidine, digoxin, benzodiazepines,
antidepressants
Withdrawal from alcohol, barbiturates, and benzodiazepines
is associated with delirium as well.
2) Metabolic alterations ,including hypoxia, hypercarbia,
hyponatremia, uremia, hepatic failure, hyperglycemia,
hypoglycemia, fever , dehydration, hypercalcemia,
hyperthyroidism, porphyria, antithyroid antibodies
(Hashimoto’s encephalopathy), and thiamine B1 and
niacin B3 deficiencies, can cause delirium
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Neurology
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Dr.
Rami
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5. DELIRIUM
3) Diffuse insults to the brain ,such as meningitis,
encephalitis, fat emboli, and disseminated
intravascular coagulation (DIC), are associated
with cognitive impairment.
4) Systemic infections , such as a urinary tract
infection, pneumonia, or sepsis
Focal cerebral disease
Mass lesions also can cause a confusional state,
especially if they are located in the frontal lobes
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Neurology
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Dr.
Rami
Abo
Ali
6. DELIRIUM
Signs and symptoms
The clinical hallmarks of delirium are decreased
attention or awareness and a change in baseline
cognition.
Symptoms include the following:
Clouding of consciousness
Difficulty maintaining or shifting attention
Disorientation
Illusions
Hallucinations
Fluctuating levels of consciousness
Dysphasia
Dysarthria
Tremor
Motor abnormalities 6
Neurology
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Dr.
Rami
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Ali
7. DELIRIUM
Diagnosis
The diagnosis of delirium is clinical. No laboratory test can
diagnose delirium.
Diagnostic criteria for delirium is as follows
1. Disturbance in attention (ie, reduced ability to direct,
focus, sustain, and shift attention) and awareness
2. Change in cognition (eg, memory deficit, disorientation,
language disturbance, perceptual disturbance)
3. The disturbance develops over a short period (usually
hours to days) and tends to fluctuate during the course of
the day.
4. There is evidence from the history, physical examination,
or laboratory findings that the disturbance is caused by a
direct physiologic consequence of a general medical
condition, an intoxicating substance, medication use, or
more than one cause.
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Neurology
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Dr.
Rami
Abo
Ali
8. DELIRIUM
Therapy :
The goal of treatment is to determine the cause of the
delirium and stop or reverse it. Components of delirium
management include supportive therapy and
pharmacologic management.
Fluid and nutrition should be given carefully because
the patient may be unwilling or physically unable to
maintain a balanced intake..
Reorientation techniques or memory cues such as a
calendar, clocks, and family photos may be helpful. The
environment should be stable, quiet, and well-lighted.
Delirium that causes injury to the patient or others
should be treated with medications. The most common
medications used are antipsychotic medications
(haloperidol ) .
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Neurology
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Dr.
Rami
Abo
Ali
9. DEMENTIA
Definition :
Dementia can be defined as a global decline in
cognitive function in clear consciousness.
One should be extremely cautious in making the
diagnosis of dementia in a delirious patient.
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Neurology
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Dr.
Rami
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Ali
10. DEMENTIA
Etiology.
Causes of dementia include Alzheimer’s disease,
Parkinson’s disease, multiple cerebral infarcts,
Huntington’s disease, frontotemporal degeneration
including Pick’s disease, dementia with Lewy bodies,
human immunodeficiency virus (HIV) infection, and
Creutzfeldt–Jakob disease.
Potentially treatable conditions that can manifest as
dementia include depression (pseudodementia),
normal-pressure hydrocephalus (NPH), subdural
hematomas, tumor, adverse drug effects, thyroid
disease, vitamin B12 deficiency, syphilis, heavy metal
intoxication, conditions causing hypersomnia (e.g.,
sleep apnea syndrome), chronic meningitis, and
Wilson’s disease.
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Neurology
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Dr.
Rami
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Ali
11. DEMENTIA
ALZHEIMER’S DISEASE.
This condition is the most common cause of chronic
dementia
Definition.
Alzheimer’s disease is a clinicopathologic entity
characterized by progressive memory loss and other
cognitive deficits.
Onset commonly is late in life, although patients
may be affected in middle age.
The disease usually arises spontaneously, but
genetic factors have been identified.
Familial cases have been associated with mutations
of the genes for amyloid precursor protein, presenilin
1, and presenilin 2.
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Neurology
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Dr.
Rami
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Ali
12. DEMENTIA
ALZHEIMER’S DISEASE
Prevalence :
It is estimated that 60%–80% of demented
patients have Alzheimer’s disease.
The prevalence increases sharply with age,
affecting 5%–15% of people older than age 65
years and about three times as many people older
than age 85 years (the fastest-growing segment
of the population).
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Neurology
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Dr.
Rami
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13. DEMENTIA
ALZHEIMER’S DISEASE
Pathology .
Although the cause and pathogenesis are unknown,
Alzheimer’s disease has a characteristic pathology
consisting of intracellular neurofibrillary tangles and
extracellular neuritic plaques.
The tangles are composed primarily of abnormally
phosphorylated, microtubule-associated tau protein.
The amyloid protein, A, is derived from amyloid
precursor protein and is deposited in senile plaques and
blood vessels.
The gene for amyloid precursor protein resides on
chromosome 21 and may be involved in familial cases.
Associated pathologic processes disturb many
neurotransmitters, particularly the cholinergic system.
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Neurology
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Dr.
Rami
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Ali
15. DEMENTIA
ALZHEIMER’S DISEASE
The clinical diagnosis of senile dementia of the
Alzheimer’s type (SDAT) can be made if an
otherwise alert patient exhibits progressive
memory loss and other cognitive deficits such as
disorientation, language difficulties, inability to
perform complex motor activities, inattention,
visual misperception, poor problem-solving
abilities, inappropriate social behavior, and,
occasionally, hallucinations.
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Neurology
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Dr.
Rami
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Ali
16. DEMENTIA
ALZHEIMER’S DISEASE
(a) The intellectual decline should be present in two or
more cognitive domains and be documented by clinical
examinations such as the Mini-Mental State
Examination
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Neurology
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Dr.
Rami
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Ali
17. DEMENTIA
ALZHEIMER’S DISEASE
(b) Formal neuropsychological testing can
confirm the clinical impression and document
progression of the disease. Tests that address
recall (with or without cues) and delayed recall
are especially sensitive for documenting early
memory impairment.
(c) Other systemic and neurologic diseases that
could produce cognitive decline should be absent.
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Neurology
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Dr.
Rami
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Ali
18. DEMENTIA
ALZHEIMER’S DISEASE
Therapy
Medical therapy is useful in treating insomnia,
agitation, and depression.
(a) In general, drugs should initially be given at a low
dose; the dose can be adjusted upward slowly as
clinically indicated.
(b) Medications with a short half-life and few
anticholinergic side effects are best tolerated.
(c) Cholinesterase inhibitors such as donepezil,
galantamine, and rivastigmine may improve cognitive
and behavioral function.
Day care centers (including day hospitals) and
respite care are useful adjuncts to family supervision
of the patient with Alzheimer’s disease and other
dementing disorders. 18
Neurology
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Dr.
Rami
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Ali
19. DEMENTIA
NORMAL-PRESSURE HYDROCEPHALUS
Definition.
NPH is a condition characterized by a triad of
cognitive impairment, urinary incontinence, and
gait apraxia (i.e., impaired ambulation without
evidence of primary motor, sensory, or cerebellar
dysfunction).
Etiology.
In most patients, the cause of NPH is unknown.
However, NPH can follow subarachnoid
hemorrhage (SAH )or meningitis, sometimes
even years later.
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Neurology
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Dr.
Rami
Abo
Ali
20. DEMENTIA
NORMAL-PRESSURE HYDROCEPHALUS
Diagnosis.
NPH should be suspected in patients who present
with the clinical features
Imaging studies
(a) CT or MRI reveals ventricular enlargement with
relatively little cortical atrophy
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Neurology
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Dr.
Rami
Abo
Ali
21. DEMENTIA
NORMAL-PRESSURE HYDROCEPHALUS
(2) In certain settings ,ICP monitoring for 24–48 hours can
reveal transient pressure increases if the diagnosis is in
doubt
Therapy.
Insertion of a ventriculoperitoneal shunt can improve the
patient’s condition, especially if performed within 6 months
of the onset of the problem.
21
Neurology
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Dr.
Rami
Abo
Ali
22. DEMENTIA
CREUTZFELDT–JAKOB DISEASE
This progressive, degenerative illness is caused by
prions (i.e., infectious proteinaceous particles) and is
associated with a spongiform encephalopathy.
The gene for the prion protein is on chromosome 20 ;
approximately 10% of cases are hereditary.
Illness can develop because of infection or somatic and
germ cell mutations .
“Mad cow disease ” probably represents transmission of
prion disease from infected cows to humans via
ingestion of bovine food products.
Patients may exhibit myoclonus .
The EEG often demonstrates bilateral periodic
discharges and an abnormal background rhythm.
Treatment is supportive. Death usually occurs within
several months of the onset of the disease.
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Neurology
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Dr.
Rami
Abo
Ali
24. HEADACHE
Headache is an extremely common complaint
that in rare circumstances may portend a life-
threatening process.
Screening for certain “red flags” may allow one to
identify high-risk individuals.
Patients suffering from the worst or first
headaches of their lives should always be
considered for further evaluation.
Similarly, elderly patients with new headaches or
patients with changes in the character of their
headaches should be seriously considered for
further evaluation. 24
Neurology
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Dr.
Rami
Abo
Ali
25. HEADACHE
ETIOLOGY
1. Non-neurologic causes :
Disorders of the head and neck such as sinus disease,
glaucoma, dental infections, temporomandibular joint
(TMJ) disease, ear pathology, muscular injury, or cervical
spine problems can cause headache.
2. Intracranial stimulation of pain-sensitive structures.
Problems that affect the meninges or distort the larger
blood vessels cause pain.
3. Life-threatening causes
a. An intracranial mass
b. Subarachnoid hemorrhage
25
Neurology
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Dr.
Rami
Abo
Ali
26. a. An intracranial mass
Causes a headache that typically develops
insidiously and progressively worsens.
Clinical features.
The pain is unlike any the patient has experienced and
may awaken the person from sleep.
Occasionally, the headache is worse in the morning.
With time, associated symptoms(e.g., nausea,
vomiting, exacerbation with lifting and straining) can
develop.
On examination, evidence of papilledema or focal CNS
disease is typically apparent.
Therapy.
Treatment is directed at the underlying lesion.
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Neurology
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Dr.
Rami
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Ali
27. b. Subarachnoid hemorrhage typically produces “the
worst headache of one’s life.”
The familiar use of the term SAH refers to
nontraumatic (or spontaneous) hemorrhage, which
usually occurs in the setting of a ruptured cerebral
aneurysm or arteriovenous malformation (AVM).
(1) Clinical features.
The possibility that a headache is a result of SAH is
strengthened if the cephalic discomfort cannot be easily
attributed to any of the usual causes of head pain. No
neurologic findings may be present on examination, and
meningismus may be absent.
The most common premonitory symptoms are as
follows:
Headache (48%) , Dizziness (10%) , Orbital pain (7%) ,
Diplopia (4%) , Visual loss (4%). 27
Neurology
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Dr.
Rami
Abo
Ali
28. (2) Diagnosis.
Given the potential seriousness of the condition,
patients should have a cranial CT scan .If this is
unrevealing, an LP documents the presence of
subarachnoid bleeding.
(3) Treatment.
Patients with SAH should undergo emergent
clipping of any offending aneurysm.
Nimodipine, a calcium channel blocker with
specific action within the CNS, should be
administered upon admission to prevent
vasospasm.
Supportive measures should be undertaken, if
necessary, with regard to ventilation and nutrition
28
Neurology
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Dr.
Rami
Abo
Ali
30. HEADACHE
1. MIGRAINE
Etiology.
The cause of migraine is unknown, but several
common precipitants have been observed.
A family history of migraine often exists.
Headaches can be related to stress, altered sleep
patterns, menses, oral contraceptives, alcohol use,
caffeine withdrawal,and various foodstuffs(e.g.,
chocolate, nuts, aged cheeses, and meats containing
nitrates).
Migraine can develop after seemingly minor head
trauma ; recognition and treatment may prevent
prolonged disability.
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Neurology
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Dr.
Rami
Abo
Ali
31. Pathophysiology.
Hypotheses center around the idea that a migraine
attack is brought on by neurovascular disturbances.
The classic vasospasm–vasodilation theory arose from
clinical observations.
Recent data suggest that oligemia, secondary to a
slowly spreading area of neuronal depolarization(the
cortical depression of Leão), occurs during a headache
prodrome and persists into the headache phase.
Hyperemia occurs subsequently and can persist after
the headache subsides.
Current theory maintains that dysfunction of the
trigeminovascular system , resulting in the
perivascular release of substance P and other
neurotransmitters and inflammatory markers, leads
to migraine.
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Neurology
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Dr.
Rami
Abo
Ali
HEADACHE
1. MIGRAINE
32. Migraine syndromes
Migraine without aura (common migraine) is a
syndrome characterized by recurrent unilateral or
bilateral headache that is throbbing in character and
worsened by movement. These headaches are often
associated with nausea, vomiting, photophobia,
phonophobia, and anorexia.
Migraine with aura (classic migraine) is a syndrome
of recurrent unilateral headaches of similar nature,
preceded by auras characterized by visual loss and
flashing lights (i.e., scintillating scotoma and
fortification spectra). Rarely, patients may suffer with
transient neurologic deficits close to stroke (e.g.,
complicated migraines). 32
Neurology
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Dr.
Rami
Abo
Ali
HEADACHE
1. MIGRAINE
33. Therapy.
Treatment should first involve the removal of
inciting agents when possible.
(1) Abortive therapy for migraine
I. Triptans , a family of serotonin 5-HT1–receptor
agonists, have become the first-line agents to abort
migraines.
II. Aspirin and other nonsteroidal anti-inflammatory
drugs (NSAIDs) are useful alternatives.
III. Ergotamine , a serotonin receptor agonist that is
available orally and in intravenous (IV)
formulations (e.g., dihydroergotamine [DHE 45]), is
currently used much less frequently.
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Neurology
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Rami
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Ali
HEADACHE
1. MIGRAINE
34. (2) Symptomatic treatment of individual
headaches is necessary if abortive measures fail.
Often patients use NSAIDS for milder headaches
but oral or parenteral narcotics for more severe
instances, such as those requiring a visit to the
emergency room. Metoclopromide is often used
an antiemetic.
(3) Prophylactic measures include medications
and lifestyle modifications.
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Neurology
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Rami
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HEADACHE
1. MIGRAINE
35. (a) Medications such as b-blockers, calcium channel
blockers, tricyclic antidepressants, NSAIDs, and
antiepileptic drugs such as gabapentin, topiramate,
and valproic acid have been used to prevent migraines.
Initially, a low dose should be administered, and the
therapeutic benefits and undesirable side effects should
be monitored as the dose is increased. The dose can be
increased until either a beneficial response is achieved or
adverse side effects develop. A maximal dose is best
maintained for several weeks before concluding that an
agent is not effective.
(b) Biofeedback therapy may enable patients to lessen
migraine events by helping them deal more effectively
with stress. 35
Neurology
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Dr.
Rami
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Ali
HEADACHE
1. MIGRAINE
36. 2. TENSION HEADACHES
Tension headaches are characterized by a band like
discomfort about the head; the pathophysiology is not
well understood, but stress is often felt to play a role.
Clinical features.
Tension headache often develops during the course
of the day, involving the posterior cervical and
occipital muscles. Distinguishing between this type
of headache and migraine without aura can be
difficult.
Therapy.
Treatment involves reassurance, NSAIDs, muscle
relaxants, moist heat, and, on occasion,
antidepressant drugs and psychotherapy.
36
Neurology
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Dr.
Rami
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Ali
37. 3. CHRONIC DAILY HEADACHE
Etiology.
Patients with migraine or tension headache
can develop chronic daily headaches
spontaneously or as a result of excessive use of
analgesics or ergotamines.
Therapy.
Treatment consists of withdrawal from
excessive medications.
Intravenous Dihydroergotamine DHE45 given
for 2–3 days can help break the headache
cycle.
Prophylactic migraine agents can help prevent
a headache recurrence.
37
Neurology
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Dr.
Rami
Abo
Ali
38. 4. CLUSTER HEADACHE
Clinical features.
Cluster headaches are severe periorbital headaches, 30–90 minutes
in duration, that occur once or several times daily over a period of
several weeks or months.
The unilateral pain may be accompanied by ipsilateral lacrimation,
conjunctival injection, nasal congestion, and Horner’s syndrome.
The typical patient is a middle-aged man. Patients with cluster
headaches often pace, as opposed to migraineurs, who seek quiet,
dark places.
The pain may be severe enough to provoke sufferers to attempt
suicide!
Therapy
Abortive and symptomatic treatment of single headaches includes
the administration of 100% oxygen, ergotamines, analgesics, or
sumatriptan .
Abortive treatment for a cluster of headaches usually consists of a
short course of corticosteroids.
Prophylactic agents may include lithium and calcium channel
blockers.
38
Neurology
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Dr.
Rami
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Ali
39. 5. TEMPORAL (GIANT CELL) ARTERITIS
a. Clinical features.
Patients older than the age of 50 years who complain of a
headache centered about one temple or located in the
occipital area should be evaluated for giant cell arteritis.
Associated symptoms include visual disturbances, jaw
claudication, fever, arthralgias and myalgias, and weight
loss. Polymyalgia rheumatica (PMR) is also present in
approximately 50% of patients with giant cell arteritis.
Diagnosis.
The erythrocyte sedimentation rate is typically greater than
40 mm/hour, and the C-reactive protein level is elevated.
Biopsy of the temporal arteries confirms the diagnosis.
Therapy.
Corticosteroid treatment can bring rapid relief but must be
maintained for many months.
39
Neurology
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Dr.
Rami
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Ali
40. 6. BENIGN (IDIOPATHIC) INTRACRANIAL
HYPERTENSION (PSEUDOTUMOR CEREBRI)
Has no known cause but is associated with
obesity, pregnancy, oral contraceptives, SLE,
cranial venous sinus thrombosis, and a host of
other conditions.
Clinical features.
The development of a relatively constant, generalized
headache in patients with a clear sensorium,
papilledema, and an otherwise normal neurologic
examination is suggestive of benign intracranial
hypertension.
Visual obscurations can occur, and visual loss is the
most serious complication.
40
Neurology
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Dr.
Rami
Abo
Ali
41. 6. BENIGN (IDIOPATHIC) INTRACRANIAL
HYPERTENSION (PSEUDOTUMOR CEREBRI)
Diagnosis.
The diagnosis is suggested by a CT or MRI scan,
showing normal or small ventricles.
The diagnosis can be confirmed by finding an
elevated CSF opening pressure and an otherwise
normal CSF analysis.
Therapy
(1) Visual acuity and fields should be monitored.
(2) Serial LP scan relieve the syndrome.
(3) Corticosteroids, acetazolamide, or furosemide may
be administered.
(4) Refractory disease has been managed with
lumboperitoneal shunting of CSF or optic nerve
sheath fenestration. 41
Neurology
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Dr.
Rami
Abo
Ali
42. 7. TRIGEMINAL NEURALGIA
Trigeminal neuralgia is a syndrome that most often
is idiopathic but has been associated with multiple
sclerosis MS, neoplasia, and purported vascular
“loops” that impinge on the trigeminal nerve (5th).
Clinical features
Lightning-quick, severe facial pains occur in the
distribution of the trigeminal nerve in the setting of an
otherwise normal exam.
The pains are classically brought on by various stimuli
such as light touch, chewing, cold substances, or wind.
Therapy.
Carbamazepine remains the first-line treatment, but
alternative treatments include baclofen, gabapentin,
surgery to remove the vascular loops , and stereotactic
radiation therapy.
42
Neurology
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Dr.
Rami
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Ali
43. 8. LOW-PRESSURE HEADACHES
Low-pressure headaches are characterized by
headaches that substantially worsen when patients
are upright and improve when supine.
Etiology.
Postural headaches typically occur after an LP but can
develop spontaneously as a result of dural tears.
Diagnosis.
MRI may show generalized dural enhancement, low-
lying cerebellar tonsils, and a “kinked” brainstem.
Therapy.
Treatment consists of a blood patch (injection of
autologous blood into the lumbar epidural space) or
repair of the dural tear. 43
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