clinical case: right sided weakness

8/20/2019 Clinical Case: Right Sided Weakness

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Pamantasan ng Lungsod ng Maynila

College of Medicine

Department of Medicine

CAMANGON, Prometheus D. June 26, 2015

3A Group 2 Dr. Alcantara

Date and Time of History Taking: June 19, 2015 - 1:30 PM

Informants: RT, grandson of the patient

Reliability: 75%

GENERAL DATA

FT, 78-year-old right-handed Filipino female, Catholic, widowed and residing at 584-120 San

Andres St. Malate, Manila. She was born on October 22, 1936. FT was admitted for the first time at Ospitalng Maynila Medical Center (OMMC) last May 14, 2015 at around 8AM.

CHIEF COMPLAINT

Right Sided Body Weakness

HISTORY OF PRESENT ILLNESS

1 day PTA. Patient collapsed after eating lunch with her relatives. Informant claimed they were

eating a high-fat meal on a hot noon. FT experienced dizziness and loss of balance after standing up and

was able to walk for 2 steps before collapsing on a step off of her right foot. The informant was able tosupport her before falling down but she lost her consciousness for 30 minutes after the incident.

Informant seek consult to a neighbor who was reported to be a medical personnel. BP was 180/90and Blood Sugar recalled at 121 mg/dL. She was advised to be admitted to the nearest hospital as soonas possible, but they were not able to comply. The informant splashed cold water to the FT, to regainconsciousness. Right-sided weakness and soft speech was noticed of FT.

12 hours PTA. Patient developed difficulty of chewing and swallowing, and she was only able toeat soft and blended foods for dinner. Her tongue was noticed to be slightly deviated to the right.

On the day of admission. Due to persistence of aforementioned observations, FT’s relativesdecided to seek consult to Ospital ng Maynila at around 8AM.

PAST MEDICAL HISTORY

There were no reported any other admission nor hospitalization. Informant was uncertain aboutpatient’s childhood illnesses and immunizations. FT was diagnosed with hypertension in 2008, and was

prescribed Metoprolol 20 mg. BP not regularly measured and highest BP was unrecalled. She take

medications during hypertensive episodes only, reported to be almost 2 times a month. Patient was also

diagnosed with cataract on both eyes, and it was surgically extracted on 2006.

Informant claimed that the patient had no regular check-up and consultation to a medical institution

or personnel. FT was also claimed to have no allergies to any food or medication, nor history of treatment

for any psychiatric disorders.



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Informant was uncertain of the patient’s screening tests and OB-Gyn History, but claimed that FT

has 3 living offsprings.

FAMILY HISTORY

Patient’s parents were both deceased, but history of hypertension was claimed by the informant.

No family history of asthma, diabetes mellitus, cancer, blood disorders, kidney disease, epilepsy, nor metal

disorders.

PERSONAL AND SOCIAL HISTORY

Informant was uncertain of the patient’s educational attainment and previous occupation. She lives

with her 6 grandchildren in a two-storey house, with proper ventilation and a pet dog. Drinking water is

purified. Garbage is segregated and collected 3 times a day and toilet utilizes flush mechanism.

FT was a smoker until 2013 (at least 21 pack-years) and drinks occasionally (2-3 bottles of beer),

but no history of illicit drug use. She had a diet preference for fatty and salty foods. Patient was also reported

to be fond of drinking carbonated drinks (4 small bottles of Coca Cola a day).

REVIEW OF S YSTEMS

Const i tu t ional : (-) Weight loss, fever and chills.

Skin : (-) Pallor. No dryness, skin and nail color changes, sores, abrasions nor ulcers

HEENT : (+) Dizziness (+) Headache. No hair loss and trauma in the head. (+) Blurring of vision. No

report any excessive lacrimation, doubling nor pain in eyes. (-) Hearing difficulty on both ears, (-)

Occasional Tinnitus, (-) Vertigo. No ear tenderness and discharge. No epistaxis, nasal discharges. No

reported dysphagia, presence of mouth sores, bleeding gums, voice hoarseness or throat soreness.

Neck: No pain, stiffness nor lumps,

Respiratory: (-) Hemoptysis nor sputum production. (-) Cough nor dyspnea

Cardiovascular: (-) Chest pain (-) Palpitations (-) Cyanosis (-) Orthopnea (-) PND

Peripheral Vascular Syst em: No leg cramps nor varicose veins.

Gastrointestinal : No reported loss of appetite, nausea, diarrhea, excessive gas belching, hematemesis

nor hematochezia.

Renal: No reports of dysuria, urinary urgency, hesitancy, dribbling, nocturia, incontinence, polyuria,

gross hematuria nor urinary retention.

Genital : No reported pain, swelling, ulcers.



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Extremities: (-) Joint Pain. No reports of muscle pain with tingling sensation nor backache.

Neurologic : No reported memory loss nor seizures.

Hemato log ic: No reports of easy bruising and overt bleeding.

Endocr ine : No reports of heat or cold intolerance, excessive sweating, polyphagia, polydipsia

Psychiatr ic : No reports of anxiety, nervousness, depression nor hallucinations.

PHYSICAL EXAMINATION

General Survey

Patient was obtunded to stupor, toxic looking and non-ambulatory. She was in a supine position,

assisted by oxygen and NGT; and hooked with an IV line of PNSS and Mannitol. She was not responsive

to any questions.

Vital Signs

Pulse rate: 64 bpm. BP 110/60, supine, right arm. Temperature was 39.0°C (left axillary).

Respiratory rate: 18 bpm.

Skin

Nail beds were not pale. No jaundice clubbing nor cyanosis. Skin was dry and warm with good

turgor. No suspicious nevi, rash, petechiae, eccyhmoses.

HEENT

Head: Head was in proportion with the body. Hair was grayish with fine strand. There were no

lesions in the scalp, deformities and tenderness of the skull. Face in asymmetrical, deviated

to the right but still was able to raise her eyebrows in response to questions. No edema,

redness, cyanosis on face.

Eyes: Eyebrows were symmetrical and evenly distributed. Eyes were symmetric and not

protruding. Symmetric eyelids without edema, ptosis, lesions or abnormal movement. No

excessive tearing or dryness. Sclera were anicteric and both conjunctiva was pale. Light

reflexes were not assessed.

Ears: Auricles were symmetric without swelling, redness, discharge. Weber’s test, Rinne’s test

and otoscopy were not assessed.

Nose: Nasal septum midline and symmetric, with no tenderness, nasal obstruction nor lesions.

Frontal and maxillary sinuses were non-tender.Mouth &

Pharynx:

Lips were dry but without any lumps nor lesions. The oral mucosa was pale with 1cm

excoriation on the right vermillion border but without ulcers, patches nor nodules. There were

also no swellings and ulcers in the soft and hard palate. Tongue was dry, with scales on the

tongue’s ventral surface, slightly deviated to the right. Anterior tonsil pillars were symmetric

without swelling or exudates. Pharyngeal tonsils were also not swollen. Uvula was not

assessed.



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Neck

Trachea was at midline. There were no palpable cervical lymph nodes enlargement. Thyroid wasnot enlarged. There was no deviation of thyroid cartilage and cricoid cartilage and the thyroid cartilage waselevated upon swallowing. Jugular venous pressure (JVP) was not assessed.

Thorax and Lungs

Posterior Thor ax

Upon inspection, chest was symmetric and flat with no lesions, abnormal retractions nor unilateral

lag. There were no tender areas nor palpable masses. Equal chest expansion and equal tactile fremitus

were exhibited after palpation. Percussion of the posterior thorax exhibited resonant notes on all lung fields.

Auscultation revealed vesicular breath sounds on all lung fields, without any adventitious sounds.

Anter ior Thorax

Upon inspection, chest was symmetric during respiration and there were no seen use of accessory

muscles in breathing. Equal chest expansion and tactile fremitus were observed during palpation. While,

auscultation revealed vesicular breath sound on all lung fields and no adventitious sounds heard. Trachealbreath sounds above the suprasternal notch. Auscultation revealed vesicular breath sounds on all lung

fields, without any adventitious sounds.

Cardiovascular

Upon inspection, the precordium was adynamic and PMI was not visible. PMI was palpated to be

3.5cm in diameter and at the level of the 5th intercostal space, 10cm lateral to the left midsternal line and

tapping in nature. There were no thrills palpated. Heartbeat was regular in rate and in rhythm. Heart sounds

are soft but S1 was louder than S2 at apex and S2 was louder than S1 at base. There were no heard S3,

S4, murmurs nor pathologic S2 split.

Abdomen

Abdomen was protuberant and symmetric with no bulges, discoloration, hernias, rashes and

lesions. Umbilicus was inverted and at midline. There were no visible veins, peristalsis, hematoma nor

pulsations. Patient’s bowel incontinence was evident throughout the interview. Auscultation revealed

hypoactive bowel sounds (4 per minute) without bruits, venous hums and friction rubs. Percussion of the

abdomen resulted into tympanitic sounds in all quadrants and liver span was 12cm midclavicular line. Liver

edge was smooth at 2cm below the right costal border. Upon palpation, the abdomen was soft, with no

involuntary muscle guarding, tenderness nor muscular resistance. Liver, kidneys and spleen were not

protruding nor palpable.

Extremities

Presence of edema on both upper extremities. [Grade 1: pitting]. No other lesions, deformities,

visible joint swelling, nor redness. ABI was not measured. Radial, popliteal and dorsalis pedis pulses wereall +2.



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NEUROLOGIC EXAMINATION

Mental Status Examination

The patient was not able to response to MMSE because her obtunded to stupor level of

consciousness.

Cranial Nerves Examin ation

Cranial nerves were not assessed due to unresponsiveness of the patient.

Motor Examinat ion

Body Posi t ion

Patient was not able to change position without assistance. The patient was also unable to sit norstand due to weakness, thus, posture was not assessed. Leaning and head facing towards her right.

Invo luntary Movements

Tremors, tics, fasciculation, clonus, spasm, and seizures were not observed on the patient.

Muscle Bulk and Tone

There was noticeable decreased muscle bulk on both the left extremities, and right arm and legwere spastic (stiff and cannot be passively moved)

Muscle Strength

Muscle strength was assessed but data was inconsistent throughout. This may be due to thespastic nature of the patient’s right extremities and her obtunded state.

Strength Right Left

Wrist extension 0/5 -Elbow flexion 1/5 -

Elbow extension 1/5 -

Knee extension 0/5 -

Knee flexion 0/5 2/5

Sensory Examinat ion

Sensory examination was not assessed due to unresponsiveness of the patient.

Reflexes

(+) Babinski reflex and (+) Right unilateral hyperreflexia

Reflexes Right Left

Biceps (C5,C6) - +2

Triceps (C6,C7) - -

Supinator (C5,C6) +4 +2

Knee (L2-L4) +4 +2

Ankle (S1) +4 +2

Plantar (L5,S1) ↑ ↓



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CASE DISCUSSION

Sal ient Features

Pertinent Positives Pertinent Negatives

Sudden right-sided hemiparesis

Dizziness and loss of balance upon standing up

Loss of consciousness after collapsing

Soft voice or speech upon gaining consciousness

History of hypertension

Non-compliant to maintenance medication

Family History of hypertension

Smoker (21 pack years) and occasionally alcoholic

Diet preference of fatty and salty food, andcarbonated drinks

ROS: (+) Headache, Blurring of vision

Non-ambulatory and only limited movement

Obtunded to stupor LOC Fever (39oC)

Pallor and blurring of vision

Face asymmetric and deviated to the right

Tongue slightly deviated to the right

Hypoactive bowel sounds and bowel incontinence

Weaker muscle strength on the right

(+) Babinski on the right

Hyperreflexia on the right

Decreased muscle bulk on left extremities

Trauma history (informant was ableto catch her when she collapsed)

Slurring of speech

Headache after the incident

Nausea and vomiting

Nuchal rigidity and Seizure

Chest pain

Pain in the eye and loss of vision

APPROACH TO DIAGNOSIS

The patient presented with right hemiparesis. Unilateral weakness can always almost be account

to be neurovascular in origin, but a thorough approach is always needed to justify the diagnosis and to

avoid missing out important points leading to the correct diagnosis and management.

Right Hemiparesis

Infectious

Meningitis

Encephalitis

Inflammatory

Multiple

Sclerosis

Neurovascular

Cerebrovascular

Disease

Ischemic

Hemmorhagic

Hypertensive

Encephalopathy

Neoplasm

Brain Tumor

Metabolic

Electrolyte

Imbalance



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Infectious disease such as Meningitis and Encephalitis can explain right-sided weakness whenever

the disease itself already invaded specific areas of the brain. They also make strong point due to the

patient’s febrile and pallor state. However, absence of signs of meningeal irritation such as nuchal rigidity

is a strong consideration for ruling out Meningitis. Although neurologic focal findings were not thoroughly

assessed, absence of personality changes and altered mental status are strong consideration for ruling out

Encephalitis as well. Thus, laboratory workups are necessary to rule out infectious origin of the disease,

but considering the data from history and PE strongly suggest so. (Longo et.al., 2015)

Metabolic disease such as hypoglycemia and hyponatremia is also a strong consideration due to

its epidemiologic factors, the patient’s history and clinical manifestation. Although most of cases present

with bilateral weakness, it may also present unilaterally and be detrimental to the patient when this

diagnosis is left out. The only lacking evidence is that it cannot be proved upon by not utilizing laboratory

exams. (Longo et.al., 2015)

Patient’s history of hypertension and non-compliance to medication strongly suggest hypertensive

encephalopathy. Stroke is a common complication of this disease, however it cannot be proven without

utilizing ophthalmoscopy of the patient. In addition with the patient not having stage 2 HTN, absence or

without the confirmation with papilledema, hemorrhage, exudates and cotton-wool spots will strongly

suggest ruling it out. (Schwartz et.al., 1992)

After narrowing down the possible cause of the patient’s signs and symptoms, it may come up tobe Multiple Sclerosis, Ischemic Stroke, Hemorrhagic Stroke and Brain Tumor; to be discussed in the

differential diagnosis.

DIFFERENTIAL DIAGNOSIS

BRAIN TUMOR

Growth of a brain tumor takes up space within the skull and interferes with normal brain activityby increasing pressure in the brain, by shifting the brain or pushing against the skull, and byinvading damaging nerves and healthy brain tissue.

Brain tumors may have a variety of symptoms ranging from headache to stroke, depending on

its location. Specifically, when a tumor invades or occupies space or occlude a specific arterysupplying certain parts of the body. This can explain the headache, dizziness and eventuallyright sided hemiparesis of the patient.

Ruled In Ruled Against

78 yo, female Headache Blurring of vision Right hemiparesis Facial asymmetry History of smoking

(-) Nausea and vomiting (-) Personality changes and drastic weight

loss Sudden onset of hemiparesis (-) History of seizures (-) Imaging evidences proving the existence

of a brain tumor

Decision: Ruled Out

MULTIPLE SCLEROSIS

MS is an immune-mediated inflammatory disease that attacks myelinated axons in the CNS,destroying the myelin and the axon in variable degrees and producing significant physicaldisability.

Sensory loss is usually an initial complaint of patients with MS, but sensory examination was notassessed in the patient due to her obtunded state. However, spinal cord symptoms such as,muscle spasticity and bowel incontinence were evident in the case.



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Cases of MS can present bilaterally or unilaterally, based on the location of the lesions whereinantibodies have destroyed. Thus, it can explain the unilateral nature of the patient symptoms aswell as other systemic symptoms.


78 yo, female

Headache Dizziness Blurring of vision Right hemiparesis Facial asymmetry History of smoking Bowel incontinence Muscle spasticity Fever

(-) Evidence pertaining to Charcot’s triad of

apraxia, dysarthria and tremor (-) Ophthalmologic examination pertaining tooptic neuritis or optic disk pallor

(-) Evidence of diplopia and gaze preference (-) Heat intolerance

Decision: Ruled Out

HEMORRHAGIC STROKE

Leakage from small intracerebral arteries are the usual cause of bleeding occurring directly intothe brain parenchyma or hemorrhagic stroke. Chronic damage on the arteries resulting them to

leak are commonly caused by poorly controlled chronic hypertension, which is evident in thiscase.

Sudden right hemiparesis and eventual focal neurologic deficits present mostly in stroke patients.Hemorrhagic stroke however, presents usually with headache, altered mental status, seizures,nausea and vomiting.

Type of deficit depends on the area of brain involved. If the dominant (left) hemisphere isinvolved, it will result into, right hemiparesis, right hemisensory loss, left gaze preference, rightvisual field cut, aphasia and neglect.

Only a few of aforementioned symptoms are consistent with the case, having the diagnosis lesslikely.


78 yo, female Headache Blurring of vision Right hemiparesis Facial asymmetry Intact bilateral upper facial strength History of smoking History of hypertension Smoking Weak speech (+) Babinski reflex on the right Hyperreflexia on right extremities

(-) Nausea and vomiting (-) Altered mental status (-) History of seizures (-) Evidence of sensory deficit (-) Evidence for visual field deficit and gaze

preference

Decision: Ruled Out

ISCHEMIC STROKE

Cerebral ischemia comprises 85% of stroke etiology, wherein there is a reduction of blood supplyin an area of the brain lasting for few seconds. Since brain tissue does not have the capacity tostore energy for its own consumption, rapid damage to the tissue occurs with decreased bloodsupply.

Ischemic stroke can be differentiated according to the common cause: Embolic stroke,triggered by an occlusion of cerebral vasculature by an emboli from a distant source;Thrombotic stroke, occlusion caused by a thrombus or clot which was formed on the walls of



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the same vessel which was occluded; Global ischemic stroke, reduction in blood pressureresulting into hypotensive stroke.

Sudden right hemiparesis and eventual focal neurologic deficits present mostly in ischemicstroke patients. Type of deficit depends on the area of brain involved. In this case, the patientpresented with dizziness and loss of consciousness, eventually leading to right upper and lowerextremity weakness, right lower facial muscles weakness and weakened speech activity.


78 yo, female Headache Blurring of vision Right hemiparesis Facial asymmetry Intact bilateral upper facial strength History of smoking History of hypertension Smoking Weak speech (+) Babinski reflex on the right Hyperreflexia on right extremities

(-) Evidence of sensory deficit (-) Evidence for visual field deficit and gaze

preference

Decision: Ruled In

WORKING DIAGNOSIS

Ischemic stroke is characterized by sudden loss of blood circulation to an area of the brain, resultingin a corresponding loss of neurologic function. In this case, it may be caused by thrombotic or embolicocclusion of a cerebral artery; while global ischemic stroke can be ruled out to the involvement of face andspeech.

Risk factors consistent with the patient are: old age, history of hypertension, smoking (21 pack-years) and non-compliance to anti-hypertensive medications. In addition with, manifestation such as abruptonset right hemiparesis, facial asymmetry, weak speech, (+) Babinski reflex on the right and hyperreflexia

on right extremities pertains also to be consistent with ischemic stroke.The informant claimed that the patient was still observed to have the ability to answer questionswith the use of her eyebrows (i.e. lifting symmetrically as a “yes”), suggesting intact comprehension andunaffected bilateral upper facial motor activity. Since the deficits were rapidly observed maximally after theincidence of dizziness, and cannot be concluded as a pure motor deficit, the ischemic stroke may beentertained as either an embolic or thrombotic event. The differentiation between the two is almost alwaysdifficult to ascertain.

The manifestations of the patient can be localized in a specific area of the brain supplied by the leftmiddle cerebral artery. This artery supplies the lateral portion of the frontal and parietal lobes, and anteriorand lateral portions of the temporal lobe. Since these locations involve the sensorimotor cortex and theBroca’s area, the presence of contralateral hemiparesis and affluent aphasia is consistent with the expectedmanifestations from the patient. Also, hyperreflexia was observed in the right extremities of the patient,which suggests upper motor neuron disorder. The presence of a positive Babinski sign is also consistentwith stroke. Other cerebral vasculatures were ruled out due to facial involvement, among others, commonlyoccurring with middle cerebral artery occlusion. Although sensory and visual deficits cannot be correlateddue to lack of information, motor deficit correlation can be more closely linked with this artery.

Cerebrovascular AccidentProbably due to Ischemic Stroke,

Left Middle Cerebral Artery in distributionStage 2 Hypertension, uncontrolled



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Chest X-Ray

This test it to assess the physical examination finding of the location of the PMI, having 9cm lateral

to the mid-sternal line. CXR can further conclude a diagnosis of left ventricular hypertrophy; without which,

we cannot rely heavily on PE results.

LABORATORY TESTS

Complete Blood Count

CBC serves as a baseline study and may reveal a cause for the stroke (eg, polycythemia,

thrombocytosis, thrombocytopenia, leukemia) or provide evidence of concurrent illness (eg, anemia).

Blood Chemistry and Blood Glucose

The basic chemistry panel serves as a baseline study and may reveal a stroke mimic (eg,

hypoglycemia, hyponatremia) or provide evidence of concurrent illness (eg, diabetes, renal insufficiency).

Lum bar Puncture

A lumbar puncture is required to rule out meningitis or subarachnoid hemorrhage when the CT

scan is negative but the clinical suspicion remains high.

Coagulation Studies

Coagulation studies may reveal a coagulopathy and are useful when fibrinolytics or anticoagulants

are to be used. In patients who are not taking anticoagulants or antithrombotics and in whom there is no

suspicion for coagulation abnormality, administration of rt-PA should not be delayed while awaiting

laboratory results.

Cardiac B iomarkers

Cardiac biomarkers are important because of the association of cerebral vascular disease and

coronary artery disease. Additionally, several studies have indicated a link between elevations of cardiac

enzyme levels and poor outcome in ischemic stroke.

TREATMENT AND MANAGEMENT

The central goal of therapy in acute ischemic stroke is to preserve tissue in the ischemic penumbra,where perfusion is decreased but sufficient to stave off infarction. Tissue in this area of oligemia can bepreserved by restoring blood flow to the compromised area and optimizing collateral flow.

Recanalization strategies, including the administration of intravenous (IV) recombinant tissue-typeplasminogen activator (rt-PA) and intra-arterial approaches, attempt to establish revascularization so that

cells in the penumbra can be rescued before irreversible injury occurs. Restoring blood flow can mitigatethe effects of ischemia only if performed quickly.

Many surgical and endovascular techniques have been studied in the treatment of acute ischemicstroke. Carotid endarterectomy has been used with some success in the acute management of internalcarotid artery occlusions, but no evidence supports its use acutely in ischemic stroke.

In addition to limiting the duration of ischemia, an alternative strategy is to limit the severity ofischemic injury (ie, neuronal protection). Neuroprotective strategies are intended to preserve the penumbral



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tissues and to extend the time window for revascularization techniques. At the present time, however, noneuroprotective agents have been shown to impact outcomes in ischemic stroke.

Thrombolyt ic Therapy

IV recombinant tissue plasminogen activator (rtPA) given 3 hours after the stroke onset. Although,there are some contraindications to thrombolytic therapy:

Another stroke or serious head injury within previous 3 months

Major surgery within the preceding 14 days

Current use of oral anticoagulants or PT<15 seconds

Use of heparin in the previous 48 hours or prolonged PTT >1.5x

Platelet count <100,000 mm3

SBP >185 mmHg or DBP >110 mmHg

Rapidly improving neurological signs

Mild, isolated neurologic deficits

Prior intracerebral hemorrhage

Blood glucose <50mg/dl or >400mg/dl

Seizure at onset of stroke

Gastrointestinal or urinary bleeding within preceding 21 days

Recent myocardial infarction within the previous 3 months(Longo et.al., 2015)

Ant ip la tele t A gents

Aspirin is given to prevent atherothrombotic events, by inhibiting the formation of interarterialplatelet aggregates – 160 to 325 mg/d within 48 hours for 14 days until discharged. Heparin can also beused but should not exceed 5,000 units BID. (Longo et.al., 2015)

Neuroprotect ive Ag ents

The rationale for the use of neuroprotective agents is that reducing the release of excitatoryneurotransmitters by neurons in the ischemic penumbra may enhance the survival or these neurons. Usual

treatment includes Citicoline 500mg/tab – 1tab 2x a day to complete 6 weeks.

Allow hypotension – allow permissive hypertension during the first week to ensure adequatecerebral perfusion.

Avoid hypoxemia – maintain adequate tissue oxygenation (target O2 sat >95%). Givesupplemental oxygen if with hypoxemia or desaturation. Provide ventilator support if upper airwayis threatened, sensorium is impaired or ICP increased.

Avoid hypoglycemia or hyperglycemia – ensure glycemic control and avoid glucose containingIV fluids like D5, use isotonic saline instead.

Avoid hyperthermia – treat fever with antipyretics and cooling blankets.(Longo et.al., 2015) (Hughes et.al. 2014)

Rehabi l i tat ion Therapy

The goal of rehabilitation program is to help relearn skills you lost when stroke affected part of yourbrain. Stroke rehab can help regain one’s independence and improve quality of life. The program consistsof numerous physical activities, technology-assisted physical activities, and cognitive and emotionalactivities.

(Hughes et.al. 2014) (Kernan et.al., 2014)

Stroke Prevention

Secondary prevention refers to treatment of individuals who have already had a stroke. Measuresmay include use of platelet antiaggregants, antihypertensives, statins and lifestyle intervention. Smoking



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cessation, blood pressure control, diabetes control, low-fat diet, weight loss and regular exercise hould beencouraged as strongly as the medications described above.

(Sare et.al., 2009) (Kernan et.al., 2014)

REFERENCES

Fauci, A. S., Kasper, D. L., Longo, D. L., Braunwald, E., Hauser, S. L., Jameson, J., et al. (2015). Harrison's

Principles of Internal Medicine. Philadelphia: McGraw Hill Companies

Schwartz RB, Jones KM, Kalina P, et.al. Hypertensive encephalopathy; findings of CT, MR imaging andSPECT imaging in 14 cases. AJR Am J Roentgenol. Aug 1992.

Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD, Borden WB, et al. Heart disease and stroke

statistics--2012 update: a report from the American Heart Association. Circulation. 2012 Jan 3.

Adams HP Jr, Davis PH, Leira EC, Chang KC, Bendixen BH, Clarke WR, et al. Baseline NIH Stroke Scalescore strongly predicts outcome after stroke: A report of the Trial of Org 10172 in Acute Stroke Treatment

(TOAST). Neurology. 1999 Jul 13. 53(1):126-31.

Kasner SE, Grotta JC. Emergency identification and treatment of acute ischemic stroke. Ann Emerg Med.

1997 Nov. 30(5):642-53.

Sare GM, Geeganage C, Bath PM. High blood pressure in acute ischaemic stroke--broadening therapeutic

horizons. Cerebrovasc Dis. 2009.

[Guideline] Hughes S. New AHA/ASA Stroke Secondary Prevention Guidelines. Medscape Medical News.

May 2 2014.

[Guideline] Kernan WN, Ovbiagele B, Black HR, et al. Guidelines for the Prevention of Stroke in Patients

With Stroke and Transient Ischemic Attack: A Guideline for Healthcare Professionals From the American

Heart Association/American Stroke Association. Stroke. 2014 May 1.

clinical case: right sided weakness

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