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![ 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.
33
Neurology
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Dr.
Rami
Abo
Ali
HEADACHE
1. MIGRAINE](https://image.slidesharecdn.com/neurology3rddeliriumdementiaheadache-210503181029/75/Neurology-3rd-delirium-dementia-headache-33-2048.jpg)
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Neurology 3rd delirium , dementia ,headache
- 1. NEUROLOGY Dr. Rami AboAli Neurology - Dr. Rami Abo Ali 1
- 2. 1) DELIRIUM ,DEMENTIA 2) HEADACHE Neurology - Dr. Rami Abo Ali 2
- 3. DELIRIUM Definition: Deliriumis 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 - Dr. Rami Abo Ali
- 4. DELIRIUM Generalized braindysfunction 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 4 Neurology - Dr. Rami Abo Ali
- 5. DELIRIUM 3) Diffuse insultsto 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 5 Neurology - Dr. Rami Abo Ali
- 6. DELIRIUM Signs andsymptoms 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 - Dr. Rami Abo Ali
- 7. DELIRIUM Diagnosis Thediagnosis 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. 7 Neurology - 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 ) . 8 Neurology - 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. 9 Neurology - Dr. Rami Abo Ali
- 10. DEMENTIA Etiology. Causesof 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. 10 Neurology - Dr. Rami Abo Ali
- 11. DEMENTIA ALZHEIMER’S DISEASE. Thiscondition 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. 11 Neurology - Dr. Rami Abo 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). 12 Neurology - Dr. Rami Abo Ali
- 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. 13 Neurology - Dr. Rami Abo Ali
- 14.
- 15. DEMENTIA ALZHEIMER’S DISEASE Theclinical 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. 15 Neurology - Dr. Rami Abo 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 16 Neurology - Dr. Rami Abo 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. 17 Neurology - Dr. Rami Abo 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 - Dr. Rami Abo 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. 19 Neurology - 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 20 Neurology - 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 - Dr. Rami Abo Ali
- 22. DEMENTIA CREUTZFELDT–JAKOB DISEASE Thisprogressive, 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. 22 Neurology - Dr. Rami Abo Ali
- 23.
- 24. HEADACHE Headache isan 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 - 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 - Dr. Rami Abo Ali
- 26. a. Anintracranial 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. 26 Neurology - Dr. Rami Abo Ali
- 27. b. Subarachnoidhemorrhage 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 - 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 - Dr. Rami Abo Ali
- 29. HEADACHE SYNDROMES 1.Migraine 2. Tension headaches 3. Chronic daily headache 4. Cluster headache 5. Temporal (giant cell) arteritis 6. Benign (idiopathic) intracranial hypertension (pseudotumor cerebri) 7. Trigeminal neuralgia 8. Low-pressure headaches 29 Neurology - 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. 30 Neurology - Dr. Rami Abo Ali
- 31. Pathophysiology. Hypothesescenter 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. 31 Neurology - 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 - Dr. Rami Abo Ali HEADACHE 1. MIGRAINE
- 33. Therapy. Treatmentshould 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. 33 Neurology - Dr. Rami Abo Ali HEADACHE 1. MIGRAINE
- 34. (2) Symptomatictreatment 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. 34 Neurology - Dr. Rami Abo Ali HEADACHE 1. MIGRAINE
- 35. (a) Medicationssuch 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 - Dr. Rami Abo 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 - Dr. Rami Abo Ali
- 37. 3. CHRONIC DAILYHEADACHE 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 - 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 - Dr. Rami Abo Ali
- 39. 5. TEMPORAL (GIANTCELL) 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 - Dr. Rami Abo 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 - 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 - 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 - Dr. Rami Abo 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 Neurology - Dr. Rami Abo Ali
- 44.