CRANIAL NERVE DISORDERS

Cranial CT: Completed InfarctionLarge cortical infarcts tend to be wedge-shaped, while small subcortical infarcts are usually round or ovoid

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Early signs of infarction on MRI Slow flow (absence of normal flow void) in involved arteryParenchymal signal changes(hypointense on T1, hyperintense on T2 and DWI)T1 T2DWI: acute infarct appears bright80Internuclear OphthalmoplegiaWhen an attempt is made to gaze contralaterally (relative to the affected eye), the affected eye adducts minimally, if at all. The contralateral eye abducts, however with nystagmus.

Additionally, the divergence of the eyes leads to horizontal diplopia. That is, if the right eye is affected the patient will "see double" when looking to the left, seeing two images side-by-side.

Convergence is generally preserved.

Internuclear OphthalmoplegiaIn older people, the disorder usually results from a stroke, and only one eye is affected. In younger people, it usually results from multiple sclerosis, and both eyes are often affected. Less common causes include Lyme disease, tumors, and toxicity due to a drug (such as tricyclic antidepressants).

Horizontal Gaze Palsymay be caused by lesions in the cerebral hemispheres, which cause paresis of gaze away from the side of the lesion,

or from brain stem lesions, which, if they occur below the crossing of the fibers from the frontal eye fields in the caudal midbrain, will cause weakness of gaze toward the side of the lesion.

Another way to remember this is that patients with hemisphere lesions look toward their lesion, while patients with pontine gaze palsies look away from their lesions.

Vertical Gaze PalsyVertical gaze decreases gradually with aging, but vertical gaze palsy is more severe than age-related changes. Usually, upward gaze is affected. The most common cause is damage to the top part of the brain stem (midbrain), usually by a stroke or tumor.

Oculomotor Nerve PalsyOculomotor nerve supplies the majority of the muscles controlling eye movements (medial rectus, superior rectus, inferior rectus, and inferior oblique). These muscles adduct, depress, and elevate the eye.

In addition, the nerve also supplies the upper eyelid muscle (Levator palpebrae superioris) and the muscles responsible for pupil constriction (sphincter pupillae) .

Symptoms: down and out position of the affected eye, diplopia, ptosis, and pupil dilation

Oculomotor Nerve PalsyEtiology/ies:Vascular disorders such as diabetes, heart disease, atherosclerosis and aneurysm (posterior communicating artery); Tumours (malignant and non-malignant); Inflammation and Infection; Trauma; Multiple Sclerosis; Myasthenia Gravis; Post-op complication of NSS; Cavernous Sinus Thrombosis

Diagnosis and Treatment:diagnosis is based on results of a neurologic examination, CT or MRI. Spinal tap, MR angiography, CT angiography may be done.Treatment depends on the cause. Emergency treatment is required if a life-threatening disorder is the cause.

Trochlear Nerve PalsyFourth nerve palsy is a condition caused by weakness or paralysis of the superior oblique muscle (abducts, depresses, and internally rotates the eye).

Because the fourth cranial nerve is the smallest and has the longest course of the cranial nerves, it is particularly vulnerable to injury.

Symptoms: Palsy of the 4th cranial nerve causes double vision, to compensate for the double-vision resulting from the weakness of the superior oblique, patients characteristically tilt their head down and to the side opposite the affected muscle.

Trochlear Nerve PalsyEtiology/ies:Often, the cause cannot be identified. The most common identified cause is a head injury, often due to a motorcycle accident. Occasionally, diabetes causes this palsy. Rarely, the cause is a tumor, an aneurysm, or multiple sclerosis.

Diagnosis and Treatment:diagnosis is based on results of a neurologic examination, CT or MRI. Spinal tap, MR angiography, CT angiography may be done.Treatment depends on the cause. Emergency treatment is required if a life-threatening disorder is the cause.

Abducens Nerve PalsyCN VI, innervates the ipsilateral lateral rectus (LR), which functions to abduct the ipsilateral eye. It has the longest subarachnoid course of all the cranial nerves; therefore, its syndromes are similar to those of the fourth nerve because of their long intracranial courses. The sixth nerve nucleus is located in the pons, just ventral to the floor of the fourth ventricle and just lateral to the medial longitudinal fasciculus (MLF). About 40% of its neurons project into the ipsilateral MLF only to cross over to the contralateral side and ascend to innervate that contralateral medial rectus subnucleus to participate in contralateral eye adduction.

Abducens Nerve PalsySymptoms:The affected eye cannot turn fully outward and may turn inward when people look straight ahead. Diplopia occurs when people look toward the side of the affected eye. Other symptoms depend on the cause. They include severe headache, accumulation of fluid (edema) in the conjunctiva, numbness in the face and mouth, loss of vision, and inability to move the eye in other directions.

Abducens Nerve PalsyEtiology/ies:Head injuries, Tumors, Multiple sclerosis, aneurysms, brain infections (meningitis, a brain abscess or a parasitic infection), complications of an ear or eye infection, Blockage of an artery supplying the nerve, as can result from diabetes, a stroke, a transient ischemic attack, or vasculitis, Wernicke's encephalopathy(commonly due to chronic alcoholism); benign intracranial hypertension, Respiratory infections (in children)Diagnosis and Treatment:diagnosis is based on results of a neurologic examination, CT or MRI. Spinal tap, MR angiography, CT angiography may be done. If symptoms suggest vasculitis, blood is withdrawn to check for signs of inflammation, such as certain abnormal antibodies (ANA, ESR, RF) in the blood.Treatment depends on the cause. Emergency treatment is required if a life-threatening disorder is the cause.

Trigeminal NeuralgiaUsually occurs in middle-aged and older people, although it can affect adults of all ages. It is more common among women.

Symptoms: The pain can occur spontaneously but is often triggered by touching a particular spot (called a trigger point) on the face, lips, or tongue or by an action such as brushing the teeth or chewing. Repeated short, lightning-like bursts of excruciating stabbing painUsually, unilateral. The pain usually lasts seconds but may last up to 2 minutes. Recurring as often as 100 times a day, the pain can be incapacitating. Because the pain is intense, people tend to wince, and thus the disorder is sometimes called a tic. The disorder commonly resolves on its own, but bouts of the disorder often recur after a long pain-free interval

Trigeminal NeuralgiaEtiology/ies:In most cases, the cause is unknown. A common known cause is an abnormally positioned artery that compresses the trigeminal nerve near where it exits the brain. Occasionally in younger people, trigeminal neuralgia results from nerve damage due to multiple sclerosis. Rarely, trigeminal neuralgia results from damage due to herpes zoster (a viral infection) or compression by a tumor.Diagnosis and Treatment:Distinguished from trigeminal neuropathy (due to compression caused by a tumor, stroke, an aneurysm, or multiple sclerosis). Trigeminal neuropathy can be distinguished because it causes loss of sensation and often weakness in parts of the face and trigeminal neuralgia does not.Anticonvulsants (carbamazepine, phenytoin, gabapentin); Baclofen; antidepressant; Nerve block; surgery

Bells PalsySymptoms: may feel pain behind the ear, then one side of the face may become weak or completely paralyzed.Wrinkling the forehead, blinking, and grimacing may be difficult or impossible. For most people, the face feels numb or heavy, even though sensation remains normal.The ear on the affected side may perceive sounds as abnormally loud (hyperacusis) because the muscle that stretches the eardrum is paralyzed. Etiology/ies:Bell's palsy may result from herpes simplex virus type 1, which causes herpes mouth infections. But the cause is sometimes unknown.

Bells PalsyDiagnosis:no specific test, usually be diagnosed based on symptoms. can be distinguished from a stroke because a stroke usually causes weakness only in the lower part of the face rather than in the entire face. EMG-NCVx-rays, magnetic resonance imaging (MRI), or computed tomography (CT) tumors, infection, skull fracturesA blood test may be done to check for Lyme disease, and a blood test and a chest x-ray may be done to check for sarcoidosis.Treatment:Corticosteroids may be used to reduce swelling of the nerve.Artificial tears, eye patch, rehabilitationWith or without treatment, most people recover completely within several months.

Hemifacial Spasmpainless involuntary twitching of one side of the face due to malfunction of the facial nerve.affects men and women but is more common among middle-aged and older women.Symptoms: Muscles on one side of the face twitch involuntarily, usually beginning with the eyelid, then spreading to the cheek and mouth. Twitching may be intermittent at first but may become almost continuous. The disorder is essentially painless but can be embarrassing.Etiology/ies:The spasms may be caused by an abnormally positioned artery or loop of an artery that compresses the 7th cranial nerve where it exits the brain stem.

Hemifacial SpasmDiagnosis:Magnetic resonance imaging (MRI) should be done to check for a tumor, other structural abnormalities, and evidence of multiple sclerosis. Usually, MRI can detect the abnormal loop of artery pressing against the nerve.Treatment:Botulinum toxin is the drug of choice. It is injected into the affected muscles. The same drugs used to treat trigeminal neuralgiacarbamazepine, phenytoin, gabapentin, baclofen, antidepressant may helpIf drug treatment is unsuccessful, surgery may be done to separate the abnormal artery from the nerve by placing a small sponge between them (vascular decompression).

Vestibulocochlear Nerve DisordersSymptoms: hearing loss, vertigo, false sense of motion, loss of equilibrium (in dark places), nystagmus, motion sickness, gaze-evoked tinnitus

Etiology/ies:Vestibular neuritis, cochlear neuritis, and acoustic neuromas/neurofibromatosis are relatively common conditions that affect these nerves.

Vestibulocochlear Nerve DisordersDiagnosis:The diagnosis is made when doctors see the spasms. Magnetic resonance imaging (MRI) should be done to check for a tumor. Treatment:Treatment depends on the cause.

Glossopharyngeal Neuralgiaa rare disorder, usually begins after age 40 and occurs more often in men. Symptoms: brief attacks of excruciating pain, affecting one side of the tongue or throat and sometimes an ear.Attacks may be triggered by a particular action, such as chewing, swallowing, talking, coughing, or sneezing. The pain may last several seconds to a few minutes and usually affects only one side of the throat and tongue. Etiology/ies:cause is usually unknown but sometimes is an abnormally positioned artery that compresses the glossopharyngeal nerve.

Glossopharyngeal NeuralgiaDiagnosis:Test done by touching the back of the throat with a cotton-tipped applicator. If pain results, apply a local anesthetic to the back of the throat. If the anesthetic eliminates the pain, the glossopharyngeal neuralgia is diagnosed. MRI is done to check for tumors.Treatment:The same drugs used to treat trigeminal neuralgiacarbamazepine, phenytoin, gabapentin, baclofen, antidepressant may helpIf drug treatment is unsuccessful, vascular decompression may de done

Accessory Nerve DisordersSymptoms: often exhibit signs of lower motor neuron disease such as diminished muscle mass, fasciculations, and partial paralysis of the sternocleidomastoid and trapezius muscles. Interruption of the nerve supply to the sternocleidomastoid muscle results in an asymmetric neckline, while weakness of the trapezius muscle can produce a drooping shoulder, winged scapula, and a weakness of forward elevation of the shoulder. Etiology/ies:Medical procedures are the most common cause of injury to the spinal accessory nerve (radical neck dissection and cervical lymph node biopsy).

Accessory Nerve DisordersDiagnosis and treatment:Eden-Lange procedure, in which remaining functional shoulder muscles are surgically repositioned, may be useful for treating trapezius muscle palsy.Failure to rapidly identify spinal accessory nerve damage may exacerbate the problem, as early intervention leads to improved outcomes.

Hypoglossal Nerve DisordersSymptoms: The tongue becomes weak on the affected side and eventually wastes away (atrophies). As a result, people have difficulty speaking, chewing, and swallowing. Damage due to amyotrophic lateral sclerosis causes tiny, subtle twitching movements (fasciculations) on the surface of the tongue.Etiology/ies:Causes include a tumor or bone abnormality at the base of the skull, a stroke, infection of the brain stem, or an injury to the neck, such as that due to surgical removal of a blockage from an artery in the neck (endarterectomy). Amyotrophic lateral sclerosis (Lou Gehrig's disease) can also damage the hypoglossal nerve.

Hypoglossal Nerve DisordersDiagnosis and treatment:Magnetic resonance imaging (MRI) is usually done to look for a tumor or evidence of a stroke. A spinal tap (lumbar puncture) may be necessary if cancer or infection is possible. Treatment depends on the cause.

PERIPHERAL NEUROPATHIESPeripheral NeuropathyDamage to nerves of the peripheral nervous system, which may be caused either by diseases of or trauma to the nerve or the side-effects of systemic illness.The four cardinal patterns of peripheral neuropathy are polyneuropathy, mononeuropathy, mononeuritis multiplex and autonomic neuropathy. The most common form is (symmetrical) peripheral polyneuropathy, which mainly affects the feet and legs.

MononeuropathyMost common cause of is by physical compression of the nerve, known as compression neuropathy (Carpal tunnel syndrome, Meralgia Paresthetica). The "pins-and-needles" sensation of one's "foot falling asleep" (paresthesia) is caused by a compression mononeuropathy (a temporary one which can be resolved merely by moving around and adjusting to a more appropriate position). Direct injury to a nerve, interruption of its blood supply (ischemia), or inflammation can also cause mononeuropathy.

Mononeuritis MultiplexSimultaneous or sequential involvement of individual noncontiguous nerve trunks, either partially or completely, evolving over days to years and typically presents with acute or subacute loss of sensory and motor function of individual nerves.

The pattern of involvement is asymmetric; however, as the disease progresses deficit(s) becomes more confluent and symmetrical, making it difficult to differentiate from polyneuropathy.

Therefore, attention to the pattern of early symptoms is important.

May also cause pain, which is characterized as deep, aching pain that is worse at night, is frequently in the lower back, hip, or leg.Mononeuritis MultiplexIt is caused by, or associated with, several medical conditions: diabetes mellitus vasculitides: polyarteritis nodosa, Wegener granulomatosis, and Churg-Strauss syndrome immune-mediated diseases like rheumatoid arthritis, lupus erythematosus (SLE), and sarcoidosis infections: leprosy, lyme disease, HIV amyloidosis cryoglobulinemia chemical agents, including trichloroethylene and dapsone rarely, the sting of certain jellyfish, such as the sea nettle

PolyneuropathyMany nerve cells in different parts of the body are affected, without regard to the nerve through which they pass. Not all nerve cells are affected in any particular case. In distal axonopathy, one common pattern, the cell bodies of neurons remain intact, but the axons are affected in proportion to their length (Diabetic neuropathy) In demyelinating polyneuropathies, the myelin sheath around axons is damaged, which affects the ability of the axons to conduct electrical impulses. The third and least common pattern affects the cell bodies of neurones directly, either the motor neurones (known as motor neurone disease) or the sensory neurones (known as sensory neuronopathy or dorsal root ganglionopathy). PolyneuropathyEffect of this is to cause symptoms in more than one part of the body, often on left and right sides symmetrically. The chief symptoms: weakness or clumsiness of movement (motor); unusual or unpleasant sensations such as tingling or burning; reduction in the ability to feel texture, temperature, and impaired balance when standing or walking (sensory). In many polyneuropathies, these symptoms occur first and most severely in the feet. Autonomic symptoms may also occur, such as dizziness on standing up, erectile dysfunction and difficulty controlling urination. PolyneuropathyUsually caused by processes that affect the body as a whole.Diabetes and impaired glucose tolerance are the most common causes. Other causes including inflammatory diseases such as lyme disease, vitamin deficiencies, blood disorders, and toxins (including alcohol and certain prescribed drugs). Most types of polyneuropathy progress fairly slowly, over months or years, but rapidly progressive polyneuropathy also occurs. The treatment of polyneuropathies is aimed at eliminating or controlling the cause, maintaining muscle strength and physical function, controlling symptoms such as neuropathic pain.Autonomic NeuropathyIs a form of polyneuropathy which affects the non-voluntary, non-sensory nervous system, affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and 2. In most but not all cases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy.Autonomic NeuropathyThe signs and symptoms of autonomic neuropathy include the following: urinary bladder conditions: bladder incontinence or urine retention gastrointestinal tract: dysphagia, abdominal pain, nausea, vomiting, malabsorption, fecal incontinence, gastroparesis, diarrhea, constipationcardiovascular system: disturbances of heart rate (tachycardia, bradycardia), orthostatic hypotension, inadequate increase of heart rate on exertionother: hypoglycemia unawareness, genital impotence, sweat disturbancesSigns and symptoms of PNSensory function: negative symptoms (numbness, tremor, and gait abnormality) and positive symptoms (tingling, pain, itching, crawling, and pins and needles)Motor function: negative symptoms (weakness, tiredness, heaviness, and gait abnormalities) and positive symptoms (cramps, tremor, and fasciculations) There is also pain in the muscles (myalgia), cramps, etc., and there may also be autonomic dysfunction. During a neurological examination:those with generalized peripheral neuropathies most commonly have distal sensory or motor and sensory loss, though those with a pathology (problem) of the nerves may be perfectly normal; may show proximal weakness, as in some inflammatory neuropathies like GuillainBarr syndrome; or may show focal sensory disturbance or weakness, such as in mononeuropathies. Ankle jerk reflex is classically absent in peripheral neuropathy.

Etiologies of PNThe causes are broadly grouped as follows:Genetic diseases: Friedreich's ataxia, Charcot-Marie-Tooth syndrome, Hereditary neuropathy with liability to pressure palsyMetabolic/Endocrine: diabetes mellitus, chronic renal failure, porphyria, amyloidosis, liver failure, hypothyroidismToxic causes: Drugs (vincristine, metronidazole, phenytoin, nitrofurantoin, isoniazid, ethyl alcohol), organic metals, heavy metals, excess intake of vitamin B6 (pyridoxine)Fluoroquinolone toxicity: Irreversible neuropathy is a serious adverse reaction of fluoroquinolone drugs Inflammatory diseases: Guillain-Barr syndrome, systemic lupus erythematosis, leprosy, Sjgren's syndrome, Lyme Disease, sarcoidosisVitamin deficiency states: Vitamin B12 (cyanocobalamin), vitamin A, vitamin E, vitamin B1 (thiamin)Physical trauma: compression, pinching, cutting, projectile injuries (i.e. gunshot wound), strokes including prolonged occlusion of blood flow, electric discharge, including lightning strikesOthers: shingles, malignant disease, HIV, radiation, chemotherapyTreatment of PNPregabalin is an anticonvulsant drug used for neuropathic pain. It has also been found effective for generalized anxiety disorder. It was designed as a more potent successor to gabapentin but is significantly more expensiveDuloxetine, a serotonin-norepinephrine reuptake inhibitor, is also being used to reduce neuropathic pain.TENS (Transcutaneous Electrical Nerve Stimulation) therapy may be effective and safe in the treatment of diabetic peripheral neuropathy. A recent review of three trials involving 78 patients found some improvement in pain scores after 4 and 6 but not 12 weeks of treatment, and an overall improvement in neuropathic symptoms at 12 weeks. (Jin DM et al, 2010) A second review of four trials found significant improvement in pain and overall symptoms, with 38% of patients in one trial becoming asymptomatic. The treatment remains effective even after prolonged use, but symptoms return to baseline within a month of treatment cessation.(Pieber K et al, 2010)Thank You!

CEREBROVASCULARDISEASENikki Rose Libarnes-Manalili, MD, FPNA

What is a Stroke?STROKE IS A BRAIN ATTACK!!!

Rapidly developing clinical symptoms and or signs of focal and at times global loss of cerebral function with symptoms lasting more than twenty four hours or leading to death with no apparent cause other than that of vascular origin.(Hatano 1976) Sudden onset of focal (or global) neurologic deficit due to an underlying vascular pathology.(SSP and PNA-SC 2009)

Transient Ischemic Attack (TIA) Acute loss of focal cerebral function with symptoms lasting for less than twenty four hours, which after adequate investigation, is presumed to be due to embolic or thrombotic vascular disease.(Warlow and Morris 1982)

A transient episode of neurological dysfunction caused by focal brain or spinal or retinal ischemia, without evidence of acute infarction in which clinical symptoms typically last less than an hour. (SSP and PNA-SC 2009)

Frequency and DemographicsAve. of 500,000 new strokes occur each year in the USA. At current trends, this number is projected to jump to one million per year by the year 2050. Men are at higher risk than women for stroke. Although stroke often is considered a disease of the elderly, 25% of strokes occur in persons younger than 65 years.

Frequency and DemographicsThe incidence of hemorrhagic stroke in the Japanese population is increased (it has been associated with westernization of the Japanese diet after World War II).The WHOs Global Burden of Stroke in 2005 reported that the prevalence in the Philippines is 14 per 1,000 people, more than the average of 75% of largest hematomaCount slice as .5, if size of hematoma is 25-75%of largest hematomaDisregard slice, if size of hematoma is 185, DBP > 110 Rapidly improving / minor symptomsSeizure at onset Head trauma within 3 mos GI or Urinary tract hemorrhage within 21 daysOn anticoagulants / heparin within 48 hrsElevated PTT / PT > 1.5 Platelet count < 100,000 Glucose < 50, > 400 Properly selected patientswithin 3 hours Dose : 0.9 mg / kg IV10 % as bolus, 90% as drip for 1 hr56 kg, femaleTotal dose = 50 mg

5 mg bolus (within 3 hrs of ictus)

45 mg as drip for 1 hour 30 % MORE LIKELY to haveminimal or no disability at 3 monthsANTI-PLATELETS

ASPIRINIn 48 hours works!Fewer recurrent strokes within 14 dayFewer deaths / dependency at 6 months (IST and CAST data, 1997)Dose: 80 325 mg / dayAntiplatelet Trialist Collaboration:145 trials with almost 100,000 patients showed 23% risk reduction for stroke, MI, and vascular death.

ANTI-PLATELETS

ClopidogrelClopidogrel vs. Aspirin in Patients at Risk of Ischemic Events (CAPRIE):19,185 patients with prior stroke, MI, or PVD given Clopidogrel 75mg/day vs. ASA 325 mg/day showed 8.7% RRR in stroke, MI, and vascular death over ASA.

ANTI-PLATELETS

CilostazolCilostazol Stroke Prevention Study (CSPS):1,095 patients with cerebral infarction at 1-6 months were given Cilostazol 100 mg BID vs. Placebo, showed RRR of 41.7%.

ANTI-PLATELETS

DipyridamoleEuropean Stroke Prevention Study 2:6,602 patients randomized to ASA 25 mg BID, Dipyridamole 200 mg BID, ASA 25 mg BID + Dypiridamole 200 mg, and placeboResults: ASA better than placebo, Dipyridamole better than placebo, combination of ASA and Dipyridamole better than either one alone

ANTI-PLATELETS

TiclodipineCanadian American Ticlodipine Study (CATS):23% RR vs. placebo for stroke, MI, or vascular death.Ticlodipine Aspirin Stroke Study (TASS)12% RR vs. ASA for stroke or death at 3 years.

ANTI-COAGULANTS

Anecdotal evidence suggests that heparin may benefit some patients with progressive stroke, especially in the vertebrobasilar system, or strokes involving only a small area of the brain that are associated with an arterial or cardiac mechanism.

ANTI-COAGULANTS

Anticoagulation is not without risk. Overall, intracranial hemorrhage occurs in 1-4% of patients who receive an anticoagulant for TIA or acute stroke. Accordingly, uncontrolled hypertension, intracranial hemorrhage, and uncontrolled bleeding at another site are contraindications to anticoagulation.

ANTI-COAGULANTS

Patients with cardioembolic strokes also may be at risk for hemorrhagic transformation. Although some evidence indicates that early heparinization is beneficial, some authors believe that patients with cardioembolic stroke should not be given anticoagulants until at least 48 hours after symptom onset because of the risk of hemorrhagic transformation (5-7 d for large cardioembolic strokes).

ANTI-COAGULANTS

Immobilized stroke patients who are not receiving anticoagulants, such as IV heparin or an oral anticoagulant, may benefit from low-dose subcutaneous unfractionated or low-molecular-weight heparin, which reduces the risk of deep vein thrombosis. The use of low-molecular-weight heparin as treatment for acute ischemic stroke has not yet been studied adequately.

NEUROPROTECTANTS

Since the ischemic cascade is a dynamic process, the efficacy of interventions to protect the ischemic penumbra also may prove to be time dependent.

Citicoline (cytidine-5-diphosphate choline) is an essential intermediate in the biosynthetic pathway of structural phospholipids which are important constituents of all biological membranes, including neuronal membranesNEUROPROTECTANTS

Data Pooling Analysis of Trials on Citicoline

Treatment of patients with moderate to severe stroke with Citicoline within 24 hours resulted in 33% odds of complete recovery at 3 months.Davalos, et al. Stroke 2002;33: 2850 - 2857BP Management in Acute Ischemic Stroke

1. Treat if with any of the ff: SBP > 220 or DBP > 120 or MAP > 130mm Hg 2. Avoid precipitous drop in BP Not > 15 - 20% of baseline MAP3. Do not use rapid acting sublingual agents e.g. SL Nifedipine 4. Use easily titratable IV anti-HPN medications e.g. Nicardipine, Hydralazine, Labetolol, Esmolol

BP = 210/120 MAP = 150 mmHg 20% of 150 = 30

Compute for the desired MAP: 150 30 = 120

The desired BP: 180/90 or 160/100

Bring down the BP to not lower than 20% of the baseline MAP.MAP = systolic + 2 (diastolic)3

Recognize stroke : History, PE and focused Neuro exam should be done immediately

Prioritize diagnostic exams in the ER

Screen for eligibility for rTPAPlain Cranial CT scan remains as the most important neuroimaging study of choice

Ascertain stroke subtype because management is different

ACUTE STROKE MANAGEMENT

IV rTPA is strongly recommended in carefully selected patients with acute ischemic stroke who can receive the medication within 3 hrs

ASA (80 325 mg) should be given to acute ischemic stroke patients within 48 hrs of symptom onset

Do not forget NEUROPROTECTION: Avoid hypoxemia, hypo-hyperglycemia, hyperthermia, hypotension, hyponatremia

ACUTE STROKE MANAGEMENT

RehabilitationPhysiotherapyOptimize muscle function: e.g., mobility, balance, coordination.Help patients deal with disabilities: e.g., correct use of a cane, walker, or brace.Supplementary devices are indicated: e.g., for feeding, dressing, and writing.RehabilitationSpeech therapyAssists in improving verbal, written, or nonverbal communication skills: e.g., for those with aphasia.Diagnose and handle swallowing deficits to minimize complications.Occupational therapyOptimize functional capacities: e.g., writing and other functions to assist in daily living (ADL)

ComplicationsProblems due to loss of mobility (joint contractures, pressure sores) Permanent loss of movement or sensation of a part of the body Bone fractures Muscle spasticity Permanent loss of brain functions Reduced communication or social interaction

Reduced ability to function or care for self Decreased life span Side effects of medicationsAspiration Malnutrition

PrognosisThe long-term outcome from a stroke depends on the extent of damage to the brain, the presence of any associated medical problems, and the likelihood of recurring strokes.22% of men and 25% of women who have an initial stroke die within a year. 51% of men and 53% of women under age 65 who have a stroke die within 8 years.

PrognosisSome survivors experience depression following a stroke; early treatment for depression can positively impact rehabilitation. Between 50 and 70% of stroke survivors regain functional independence; the sooner rehabilitation begins, the greater the chance of leading a productive life. Between 15 and 30 percent of stroke survivors experience permanent disability. 20% require institutional care at three months after onset.

Last September 1999, the former Health Secretary Alberto G. Romualdez said in a press release that the cost of treating uncomplicated stroke for 5-7 days range from Php 15,000 to Php 20,000 making it not only a burden emotionally but also economically to the family and community.

Thank You! Treatment and Preventionof StrokeInfarct

Thrombotic

Embolic

Hemorrhage

ICH

SAH

Temporal ProfileRisk FactorsHPNDMSmokingHyperlipidemiaAgeHeart DiseaseACUTE STROKE MANAGEMENT CATEGORIES1. MEDICAL SUPPORT2. THROMBOLYSIS3. ANTI-COAGULATION4. ANTI- PLATELET AGENTS5. NEUROPROTECTIONI. MEDICAL SUPPORT *BP controlSBP > 220DBP > 120MAP > 130

MAP = S + 2D / 3not > 20 % of MAPExceptions:LVFAMIAortic Dissection*DrugsNicardipine

Nitroprusside

Esmolol / Labetolol

Hydralazine (?)*FeverIncrease brain damage

Treat the source

ParacetamolBlood Sugar

Treat Hyperglycemia > 180II. THROMBOLYTIC THERAPYThrombolytic TherapyrTPAStreptokinaseGolden period 3 hoursGuidelines:BP < 180 / 220CT no bleedmild and severe are not treated III.ANTI-COAGULATIONANTI- COUAGULATIONHeparin- carotid a occlusion- basilar a thrombosis- fluctuating exam

LMWH

ASAIV. ANTI-PLATELET AGENTSANTI-PLATELET AGENTSASA 80 325 mg

Dypiridamole

ESPS 2 resultsASA > placeboDypiridamole > placeboASA + Dypiridamole > than each aloneClopidogrel CaprieClaireCilostazolTriflusalTACIPEmbolicCoumadinINR 2 to 3metal values 3 to 4.5V. NEUROPROTECTIONNeuroprotectorsDexa NO

Mg SO4

Hypothermia

Barbiturate Coma

Citicoline

PiracetamSurgical ManagementCarotid NASCET

Craniotomy

VentriculostomyOTHER MODES OF MGT.StatinsSPARCL80mg Atorvastatin Stroke and TIAfor 4731 patientsLDL-C

Results: 16% reduction in stroke; 20% reduction in cardiovascular eventsOTHER MODES OF MGT.Side Effects: 1. Myopathy2. > liver enzyme3. Hemorrhage DoseACE inhibitors

ARBI

ICHHPNLocationSizea x b x c / 3 (mm)

Golf ball = 30 to 40 cc

Increase ICPMannitolHyperventilationRaise HeadRICH trialSurgical Immediate Cerebellar Hemmorhage > 3 cm

Brainstem comprssionVentricular obstructionLarge lobar

Poor outcomeAge

Deep hemorrhage

Ventricular extension

Large volume

Coexisting diseaseSAHHeadacheNape painPrognosis: vasospasm re-ruptureMEDICAL MANAGEMENT:MANNITOLDEXAMETHASONETRIPLE H hypertension, hemodilution, hypo-volemic therapyNIMODIPINESAHSURGICAL MANAGEMENT:CLIPPINGCOILINGPrognosticationPrognosis by Neuro Exama. Day of Presentation: corneal, pupillary, and occulocephalic responses1) Absence of 1 of the 3: 95% vegetative / severely disabled2) Absence of 2 of the 3: 99% vegetative / severely disabled

b. Day 1:1) Spontaneous Eye Movements: 99% w/o will be vegetative / severely disabled2) Motor Withdrawal to pain: 90% w/o will be vegetative / severely disabledc. Day 3:1) Motor Withdrawal: 100% w/o will be vegetative / severely disabled2) Spontaneous Eye Opening: (+) withdrawal but eyes closed 80% will be vegetative / severely disabledPrognosticationPrognosticationDay 7:1) Spontaneous Eye Opening: (+) withdrawal but eyes closed 100% will be vegetative / severely disabled2) Obeying Commands: (+) eye opening, dont follow commands 80% will be vegetative / severely disabledThank you!HEADACHES

147Pain-Sensitive Structuresof the HeadVenous sinuses Dural arteriesProximal 50% of the larger arteries of the circle of Willis Dura at the base of the brainAll extracranial structures148Brain parenchymaEpendymaChoroid PiaArachnoidDura over convexitySkull Pain-Insensitive Structuresof the Head149General Mechanisms of HeadacheTraction on major intracranial vesselsDistention and dilation of intracranial arteriesInflammation near pain sensitive structuresDirect pressure on cranial or cervical nervesSustained contraction of scalp or neck musclesStimulation from disease of eye, ear, nose and sinuses150Epidemiology60-75% of adults have at least one headache / year5-10% will seek physician evaluation2.8 million annual emergency room visits for headache (U.S. statistics) Less than 10% of emergency room patients with chief complaint of headache will have emergent secondary cause151Classification of HeadachesPrimary headache disorders

Secondary headache disorders152EpidemiologyTension MigraineCluster

69% 15%0.1%Primary HeadacheLifetime PrevalenceHangover FeverMetabolic disorderDisorders of nose/sinusesHead traumaDisorders of eyesVascular disorders

72% 63%22%15%4%3%1%Secondary Headache153Approach to a Patient with HEADACHE154How to approach the patientwith a headacheNeed to distinguish primary from secondary headache disorders

This can be done by obtaining an accurate history and performing a focused physical exam.155Questions to Ask in Obtaining a Headache HistoryIs this your FIRST or WORST headache? How bad is your pain on a scale of 1 to 10? Do you have headaches on a regular basis?When did this headache begin? How did it start (gradually, suddenly, other)?

156Questions to Ask in Obtaining a Headache HistoryWhere is your pain? Does the pain seem to spread to any other area? If so, where? What kind of pain do you have (throbbing, stabbing, dull, other)?

157Questions to Ask in Obtaining a Headache HistoryDo you have other medical problems? If so, what? Do you take any medicines? If so, what? Do any of your family members have headaches?

158Performing the physical examThe primary purpose of the physical examination is to identify causes of secondary headachesOnly a minority of headaches are secondary, but this category contains the most life -threatening conditions

159Performing the physical examPE should include vital signs, cardiovascular, head, and neck examinationsA complete neurologic examination is essential (including funduscopic exam)

160Performing the neurological exammental statuslevel of consciousnesscranial nerve testingpupillary responsesfunduscopic exammotor strength testingdeep tendon reflexessensationpathologic reflexes (e.g. Babinski's sign)cerebellar function and gait testingsigns of meningeal irritation (Kernig's and Brudzinski's signs)

161Funduscopic exam

Papilledema

162Diagnostic AlarmsOnset after age 50Sudden onsetIncreased frequency and severityNew onset with risk factors for HIV or cancerAssociated with systemic illness (fever, meningismus, rash)Altered consciousness or focal neurologic deficitsPapilledemaSignificant trauma

163Warning Signs Suspected recent subarachnoid hemorrhage or meningitisOther abnormal neurological signshemiparesisdiplopiaataxiaDecrease in visual acuity or temporary loss of vision164Warning SignsPersistent or increasing vomitingSeizuresEndocrine disturbances (e.g. acromegaly, diabetes insidipus, amenorrhea, galactorrhea, impaired male sexual function or beard growth and poor growth in children)165Overall ApproachChief Complaint: HEADCHEHeadache AlarmsEvidence of serious headache disorder by history or physical examDiagnosis ofPrimary Headache Disorder Work-up to identify/exclude Secondary Headache etiologyTreat Primary HeadacheNOYESYESNOConsider work-up for secondary headache166Primary headache is the illness itself167Primary headachesMost common type Have no organic causeUsually recurrentNormal neurologic examKey to correct diagnosis is the history168The Primary Headache DisordersI. MigraineII. Tension-type headacheIII. Cluster headache169Primary headachesDifferentiated byDurationFrequencyLocationSeverityQuality of pain170MIGRAINE HEADACHEMigraine headachesUnilateralThrobbing painModerate to severeAggravated by movement4-72 hoursNausea +/- vomitingPhotophobia

172Types of MigraineMigraine without aura (common migraine)Migraine with aura (classical migraine)173Migraine VariantsOphthalmoplegiaHemiplegiaComplicatedPhases of MigrainePremonitory phaseAura phaseHeadache phaseResolution phase175MigraineOccurs in more than 50% of casesOccurs hours to days before the headacheThe features are psychological, neurological and autonomic Reflects limbic/hypothalamic dysfunctionPremonitory Phase176MigrainePsychologicalPremonitory PhaseNeurological Stiff neckPhotophobiaPhonophobiaOsmophobiaConcentration difficultyYawningAutonomicAnorexiaFood cravingThirstConstipationUrinationCold feelingDepressionSluggishnessEuphoriaHyperactivityHypertalkative-nessDrowsiness177MigrainePresent in classical migraineDevelops in > 4 minutes, lasts less than one hourCharacterized by visual, sensory, motor, language and brainstem dysfunctionsDevelops headache within one hour after end of auraAura Phase178MigraineHemicranialGradual onsetThrobbingModerate-severeDuration of 4 72 hoursAggravated by physical activityAssociated features Related to trigeminovascular eventsHeadache Phase179MigraineThe patient feels bad or good after disappearance of the headacheResolution Phase180The Modified Diagnostic Criteria of Migraine of the International Headache Society (IHS)181Migraine without auraA.At least 5 attacks fulfilling B-DB.Headache lasting 4-72 hoursC.At least two of the following:1. Unilateral location2. Pulsating quality3. Moderate to severe intensity4. Worsened by physical activityD.At least one of the following: nausea,vomiting, photophobia, phonophobiaE. Secondary headache is ruled out182Migraine with auraA.At least 2 attacks fulfilling BB.At least 3 of the following:1. One or more fully reversible aura2. At least one aura symptom develops gradually over more than 4 minutes3. No single aura lasts longer than 1 hour4. Headache follows aura within 1 hour of the end of auraC. Secondary headache is excluded183Trigger Factors of MigrainePsychological

Physical Hormonal Changes Sexual activityChanges in sleep Fatigue StressTensionAnxietyLetdown184Trigger Factors of MigraineEnvironmentalBright light Odors High altitude Temperature/weather changesDietary Alcohol Certain foods Missed or delayed meals185Management of MigraineBehavioral modificationsHeadache treatmentA. AbortiveB. Preventive186Migraine managementRegularization of meals, sleep, exerciseAvoidance of migraine triggersAvoidance of overuse of analgesicsStress managementBehavioral Modifications187Migraine managementAbortive PharmacotherapyErgotamineSumatriptanZolmitriptanChlorpromazineProchloperazineDexamethasonePrednisoneKetorolacNaproxenStarting doses1-2 mg PO25-100 mg PO6 mg SC25-50 mg IV/IM5-10 mg IV/IM4-8 mg PO40-100 mg PO30-60 mg IM250-750 PO 6 mg 300 mg 12 mg 400 mg 40 mg 32 mg 200 mg 120 mg 1500 mgMaximum doses188Migraine managementPreventive PharmacotherapyPropranololMetoprololFlunarizineDivalproexMethysergideTolfenamic acidTopiramate 40 mg PO50 mg PO5 mg PO250 mg PO2mg PO100 mg PO25 mg PO320 mg450 mg10 mg3,000 mg40 mg600 mg200 mgStarting dosesMaximum doses

189Migraine managementIndications of Preventive therapyDiagnosis of migraineAcute therapy is needed more than 2x per weekAcute therapy is ineffective, intolerable, contraindicated2 or more attacks/month that produce disability for > 3 daysHeadache is associated with neurologic deficitAttacks occur in predictable pattern

190TENSION-TYPE HEADACHESTension-Type HeadachesBand-like, bilateralTightness/pressure/ dull acheRadiates to neck and shouldersMild to moderateNot aggravated by movement30 min to several days

192Tension-Type Headache (TTH)Previous LabelsTension headachePsychogenic headacheMuscle contraction headache

193Tension-type headacheTypes Episodic tension-type headache Chronic tension-type headache TTH associated with disorder of pericranial musclesTTH unassociated with disorder of pericranial muscles

194Tension-type headacheIHS Diagnostic Criteria A. At least 2 of the following:1. Pressing, tightening2. Mild to moderate severity3. Bilateral location4. No aggravation by routine physical activityB. Both of the following:1. No nausea or vomiting2. No photo/phonophobia, or one of them is presentC. At least one of the following:1. No cause for secondary headache2. If one is present, the onset of the TTH is not in close temporal relation to it195Tension-type headacheManagementA. Pharmacological therapy1. Abortive2. PreventiveB. Non-pharmacologic therapy1. Psychophysiologic2. Physical196Management of TTHAbortive PharmacotherapyAnalgesics: paracetamolNSAIDs : aspirin, indomethacin, naproxen, ketorolacCombination: analgesic + caffeine +/- butalbitalMuscle relaxants : no proven value

197Management of TTHIndications for preventive pharmacotherapyHeadache frequency of > 2x per weekHeadache duration of > 3-4 hoursHeadache severity that leads to disability and overuse of abortive drugs

198Management of TTHTricyclic antidepressantsSelective serotonin re-uptake inhibitorsMigraine preventive drugs

Preventive Pharmacotherapy199CLUSTER HEADACHESCluster headachesUnilateralHot poker/ stabbing painExcruciating Autonomic dysfunctionRestless15 min to 3 hours

201Clinical Features of Cluster HeadacheStriking periodicity: cluster starts in the same season; headache starts at the same time Stereotypical features: same side, same locationPain : excruciating, deep, boringAssociated features: autonomicHeadache frequency: usually 1-2/dayHeadache duration: 30-180 minutesCluster periods: 1-2/yearCluster duration: 1 week 1 year202Management of Cluster HeadacheAbortive treatmentPreventive treatmentAvoidance of triggersSurgery of the trigeminal ganglion

203Cluster HeadacheAbortive treatment100% O2 at 7-10 L/min. for 15 minsSumatriptan 6 mg SCDihydroergotamine 1mg IV/IM4-6 % Lidocaine, nasally

204Cluster HeadachePreventive treatmentVerapamil 120-480 mgErgotamine 3-4 mg/dayLithium carbonate 300 mg BIDMethysergideValproateCorticosteroids

205Secondary headache is the symptom206Secondary HeadachesCertain features of the history will make you suspect secondary headachePhysical exam will be abnormalFocal neurologic findingsSigns of infectionEvidence of head trauma

207Secondary HeadachesFindings on history First or worst HA everSudden-onset headacheIncrease frequency & severity of usual HAAge > 40 years oldIncrease in pain with coughing, sneezing, strainingWakes patient from sleep or disturbs sleep208Secondary HeadachesFindings on historyHIV +History of cancerHistory of head traumaSymptoms of infectionFever, nausea, and vomitingPhotophobia Stiff neck209Secondary Headaches Findings on PEunilateral loss of sensationunilateral weaknessunilateral hyperreflexiasigns of infection

210Secondary HeadachesFindings on PEHead traumaPapilledemaChanges in mental statusAtaxia

211Red Flags on historyOnset after age 40 Temporal arteritisMass lesionIncrease frequency and severitySubdural hematomaMass lesionMedication overuse212Red Flags on historySudden onset of headacheSubarachnoid hemorrhageVascular malformationMass lesion or hemorrhage into mass lesion

213Red Flags on historyHistory of head traumaIntracranial hemorrhageSubdural hematomaEpidural hematomaPost-traumatic headache

214Red Flags on historyHistory of HIV or cancerMeningitisBrain abscessMetastasisOpportunistic infection

215Red Flags on PEPapilledemaMeningitisMass lesionPseudotumor cerebri

216Diagnostic StudiesComputerized tomographyHemorrhage, tumor, abscess, AVMLumbar punctureHemorrhage, infection, increased CSF pressureMRI, MRA, or Angiography as indicatedLaboratory studies based on suspected etiologiesESR: Temporal arteritisCarboxyhemoglobin: Carbon monoxide 217Thank You!HEADACHES

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