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1 ST MODULE REPORT “HEMIPARESE” GROUP 15 NEUROPSYCHIATRY SYSTEM MEDICAL FACULTY MOSLEM UNIVERSITY OF INDONESIA 2015

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LAPORAN MODUL 1 NYERI SENDI KELOMPOK 11

1ST MODULE REPORTHEMIPARESEGROUP 15

NEUROPSYCHIATRY SYSTEM

MEDICAL FACULTY

MOSLEM UNIVERSITY OF INDONESIA

2015

PERSONALIA

TUTOR:

dr. Marlianty, Sp. M

MEMBERS:

Andi Fikrah Muliani110 213 086

Lesthary Kadir110 213 114

Khaerunnisa A.Y.110 213 094

Siti Shahrina T.A.110 213 099

A. Nur Qalby T.S.M110 213 117

Andi Azizah Noor110 213 120

Erza Alifianda110 213 129

Andy Billa Vini F.A.110 213 123

Ikram Hanafi110 213 131

Andi Nurul Fasty Batari110 213 136

SCENARIO

A woman 56 years old experienced suddenly the weakness of left body and right facial droop since 2 days ago, headache and vomiting. One moment after experiencing weakness of left body, the patient is difficult to communicate and looked sleepy.

DIFFICULT WORDS

Facial droop: stiffness/ parese of half face.

Weakness: reduction of normal power of muscle.

Looked sleepy: Samnolent, low consciousness

KEYWORDS

Woman, 56 years old

Sudden weakness of left body

Right facial droop

Headache

Vomiting

Difficult to communicate

Looked sleepy

QUESTIONS:

What is the anatomy and physiology of the related system by case?

Why did the patient get a sudden weakness in left than the facial droop in right?

How did the patient get a headache and vomiting related by this case?

Why did the patient looked sleepy and difficult to communicate?

What are the diagnostic procedures?

What are the differencial diagnoses and the complications of each differential diagnoses?

What are the treatments given to the patient?

How to prevent this disease?

What are the risc factors related by this case?

What is the Islamic perspective related to this case?

1. What is the anatomy and physiology of the related system by case?

The Nerve System

The Central Nerve System

The Peripheral Nerve System

Enchepalon

Medulla Spinalis (Spinal Cord)

Nn. Cranialis (12 pair)

N. Spinalis (31 pair)

Otonom (Involunter)

Parasymphatis

Symphatis

Cerebrum

Cerebellum

Truncus Cerebri

Mesenchepalon

1. Sehati, Nouzhan.Brain and Spine Surgery. University of California, Los Angeles (UCLA) Medical Center.

2. http://www.le.ac.uk/pa/teach/va/anatomy/case3/frmst3.html

The Anatomy of Nerve System

1. Sehati, Nouzhan.Brain and Spine Surgery. University of California, Los Angeles (UCLA) Medical Center.

2. http://www.le.ac.uk/pa/teach/va/anatomy/case3/frmst3.html

Cranial Nerve

Cranial nerve I (Olfactory nerve): Smell

Cranial nerve II (Optic nerve): Vision

Cranial nerve III (Oculomotor nerve): Eye movements and opening of the eyelid

Cranial nerve IV (Trochlear nerve): Eye movements

Cranial nerve V (Trigeminal nerve): Facial sensation and jaw movement

Cranial nerve VI (Abducens nerve): Eye movements

Cranial nerve VII (Facial nerve): Eyelid closing, facial expression and taste sensation

Cranial nerve VIII (Vestibulocochlear nerve): Hearing and sense of balance

Cranial nerve IX (Glossopharyngeal nerve): Taste sensation and swallowing

Cranial nerve X (Vagus nerve): Heart rate, swallowing, and taste sensation

Cranial nerve XI (Spinal accessory nerve): Control of neck and shoulder muscles

Cranial nerve XII (Hypoglossal nerve): Tongue movement

1. Sehati, Nouzhan.Brain and Spine Surgery. University of California, Los Angeles (UCLA) Medical Center.

2. http://www.le.ac.uk/pa/teach/va/anatomy/case3/frmst3.html

The Physiology of Nerve System

The Nerve Impulse

1. Sehati, Nouzhan.Brain and Spine Surgery. University of California, Los Angeles (UCLA) Medical Center.

2. http://www.le.ac.uk/pa/teach/va/anatomy/case3/frmst3.html

2. Why did the patient get a sudden weakness in left than the facial droop in right?

PATOMECANISM

LESI IN THE BRAIN

BLOOD SUPPLIES REDUCED

THE DISTURBANCE OF NERVE MOTOR IN BRAIN

LACK HALF OF BODY

CLINICAL MANIFESTATION

HEADACHE

THE EYES AWAY

NAUSEA AND VOMITING

SLEEPY

3. How did the patient get a headache and vomiting related by this case?

Headache

Guyton and Hall. 2006. Textbook of Medical Psycology 11th Edition. Philadelphia: Elsevier

Stimulation of pain receptors in the cerebral vault above the tentorium

Initiates pain impulses in the cerebral portion of the 5th nerve

Headache

Vomitting

The sensory signals that initiate vomiting originate mainly form the pharynx, esophagus, stomach, and upper portions of the small intestines.

From here, motor impulse that cause the actual vomiting are transmitted from the vomiting center to the way of the 5th, 7th, 9th, 10th, and 12th cranial nerves to the lower tract, and through spinall nerves to the diaphragm and abdominal muscles

Guyton and Hall. 2006. Textbook of Medical Psycology 11th Edition. Philadelphia: Elsevier

4. Why did the patient looked sleepy and difficult to communicate?

Looked sleepy and difficult to communicate

loss of blood flow to one or more regions of the brain

Low of oxygen and important nutrients

Brain cell death

Loss of consciousness and aphasia (brocas aphasia/ wernickes aphasia/ global aphasia)

5. What are the diagnostic procedures?

ANAMNESIS / HISTORY TAKING

PHYSICAL EXAMINATION

SUPPORTING EXAMINATION

Glass, Alan, M.D. and Allyson R. Zazulia, M.D. 2011. Lecture Notes of Clinical Skills: Neurological Examination. Accessed from http://neuro.wustl.edu/files/3913/4461/1673/Neurological_Exam_Lecture_Notes.pdf June 1st 2015

I. Mental Status.

A. Level of consciousness

B. Attentiveness.

C. Orientation.

D. Speech and language.

Listen to patients verbal output: motor ability to produce words, quantity of

E. Memory.

F. Higher intellectual function.

II. Cranial Nerves.

A. CN I Olfactory.

B. CN II Optic.

C. CN III, IV, VI Oculomotor, Trochlear, Abducens

D. CN V Trigeminal.

E. CN VII Facial.

F. CN VIII Acoustic.

G. CN IX & X Glossopharyngeal & Vagus.

H. CN XI Spinal Accessory.

I. CN XII Hypoglossal.

Glass, Alan, M.D. and Allyson R. Zazulia, M.D. 2011. Lecture Notes of Clinical Skills: Neurological Examination. Accessed from http://neuro.wustl.edu/files/3913/4461/1673/Neurological_Exam_Lecture_Notes.pdf June 1st 2015

III. Motoric System

IV. Reflexes.

A. Muscle stretch reflexes.

a. Biceps (C5, C6; musculocutaneous nerve).

b. Triceps (C6, C7; radial nerve) .

c. Knee (L2, L3, L4; femoral nerve).

d. Ankle (S1, S2; tibial nerve).

B. Test for clonus

C. Assign grade on scale of 0-4.

0 Absent

1 Hypoactive

2 Normal

3 Brisk/hyperactive

4 Markedly hyperactive with clonus and/or spreading

D. Plantar response (L4-S2, especially S1; tibial nerve).

Glass, Alan, M.D. and Allyson R. Zazulia, M.D. 2011. Lecture Notes of Clinical Skills: Neurological Examination. Accessed from http://neuro.wustl.edu/files/3913/4461/1673/Neurological_Exam_Lecture_Notes.pdf June 1st 2015

V. Sensory System.

A. General points.

B. Vibration.

C. Joint position sense.

D. Pain.

E. Temperature.

F. Light touch.

G. Double simultaneous stimulation (test for extinction/tactile neglect).

H. Graphesthesia (integrative sensation).

I. Stereognosis (integrative sensation).

J. Romberg.

Glass, Alan, M.D. and Allyson R. Zazulia, M.D. 2011. Lecture Notes of Clinical Skills: Neurological Examination. Accessed from http://neuro.wustl.edu/files/3913/4461/1673/Neurological_Exam_Lecture_Notes.pdf June 1st 2015

VI. Coordination.

A. Truncal stability.

B. Fine finger movements (finger tapping).

C. Toe tapping.

D. Finger-nose-finger.

E. Heel-knee-shin.

F. Rapid Alternating Movements.

VII. Station and Gait.

A. Observe the patient do the following:

1. Rise from a seated position.

2. Walk across room, turn, and come back.

3. Walk on toes.

4. Walk on heels.

5. Walk heel to toe (tandem gait) in a straight line. (Many otherwise normal elderly people cannot perform this task.)

Glass, Alan, M.D. and Allyson R. Zazulia, M.D. 2011. Lecture Notes of Clinical Skills: Neurological Examination. Accessed from http://neuro.wustl.edu/files/3913/4461/1673/Neurological_Exam_Lecture_Notes.pdf June 1st 2015

B. Be prepared to catch the patient if necessary

C. Pay attention to the following:

1. Posture of body and extremities

2. Length, speed, and rhythm of steps.

3. Base of gait (how far apart are the legs).

4. Arm swing

5. Steadiness.

6. Turning

VIII. Meningeal Signs.

A. Ask patient to flex and extend neck.

B. Passively flex and extend patients neck.

C. Observe for palpable stiffness on either active or passive movement.

Glass, Alan, M.D. and Allyson R. Zazulia, M.D. 2011. Lecture Notes of Clinical Skills: Neurological Examination. Accessed from http://neuro.wustl.edu/files/3913/4461/1673/Neurological_Exam_Lecture_Notes.pdf June 1st 2015

6. What are the differencial diagnoses and the complications of each differential diagnoses?

NON HEMORRAGIC STROKE

Stroke non hemorrhagic

Definition :

Neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours (WHO)

Etiology :

-Embolism (the clot is from other part of the body, usually cardiogenic embolism)

-Thrombosis (Obstruction of blood vessel by a clot that formed locally)

Wade S. Smith, S. Claiborne Johnston, J Donald Easton. Cerebrovascular Disease. Harrison : The Principles of Internal Medicine vol.4. Chapter 370.

Patogenesis

Occlusion (partial or complete) decreasing of PO2 and increasing of PCO2 Lactic acid increased (oxidative process is replaced by the anaerob process causing toxicity environment Vasoparalysis Nerve cells damaging Swelling of nerve fibers and myelin Irreversible damage (necrosis) Brain tissue edema Increasing intracranial pressure

If its only transient ischemic attack, the plaque may disintegrated into small piece, and the obstructed blood vessel will be recirculated.

Wade S. Smith, S. Claiborne Johnston, J Donald Easton. Cerebrovascular Disease. Harrison : The Principles of Internal Medicine vol.4. Chapter 370.

Symptoms

The symptoms only occured in one side of the face and one side of the body. The side of the face that is being affected is ipsilateral with the location of the lesion, while the side of the body that is being affected contralateral with the side of the lesion (due to the decussatio pyramidalis)

If the area of the brain affected contains one of the three prominent central nervous system pathwaysthe spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include:

hemiplegia and muscle weakness of the face

numbness

reduction in sensory or vibratory sensation

initial flaccidity (reduced muscle tone), replaced by spasticity (increased muscle tone), excessive reflexes, and obligatory synergies.

Wade S. Smith, S. Claiborne Johnston, J Donald Easton. Cerebrovascular Disease. Harrison : The Principles of Internal Medicine vol.4. Chapter 370.

Symptoms

If the location is in the brainstem, it will affect the twelve cranial nerves. Therefore it can produce symptoms relating to deficits in these cranial nerves:

altered smell, taste, hearing, or vision (total or partial)

drooping of eyelid (ptosis) and weakness of ocular muscles

decreased reflexes: gag, swallow, pupil reactivity to light

decreased sensation and muscle weakness of the face

balance problems and nystagmus

altered breathing and heart rate

weakness in sternocleidomastoid muscle with inability to turn head to one side

weakness in tongue (inability to stick out the tongue and/or move it from side to side)

Wade S. Smith, S. Claiborne Johnston, J Donald Easton. Cerebrovascular Disease. Harrison : The Principles of Internal Medicine vol.4. Chapter 370.

Symptoms

If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms:

aphasia (difficulty with verbal expression, auditory comprehension, reading and/or writing; Broca's or Wernicke's area typically involved)

dysarthria (motor speech disorder resulting from neurological injury)

apraxia (altered voluntary movements)

visual field defect

memory deficits (involvement of temporal lobe)

hemineglect (involvement of parietal lobe)

disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)

lack of insight of his or her, usually stroke-related, disability

Wade S. Smith, S. Claiborne Johnston, J Donald Easton. Cerebrovascular Disease. Harrison : The Principles of Internal Medicine vol.4. Chapter 370.

Symptoms

If the cerebellum is involved, the patient may have the following:

altered walking gait

altered movement coordination

vertigo and or disequilibrium

The symptoms of nausea and vomiting usually more typicall in the hemorrhagic stroke due to the sudden increase of intracranial pressure.

Wade S. Smith, S. Claiborne Johnston, J Donald Easton. Cerebrovascular Disease. Harrison : The Principles of Internal Medicine vol.4. Chapter 370.

Diagnostic procedure

CT Scan and MRI will provide the best imaging of the exact location of the lesion and the blood vessels that involved in the stroke attack.

Wade S. Smith, S. Claiborne Johnston, J Donald Easton. Cerebrovascular Disease. Harrison : The Principles of Internal Medicine vol.4. Chapter 370.

Management of Therapy

-Anti coagulan : Heparin and Warfarin natrium

-Anti trombosit : Aspirin

-Anti edema : Mannitol

Wade S. Smith, S. Claiborne Johnston, J Donald Easton. Cerebrovascular Disease. Harrison : The Principles of Internal Medicine vol.4. Chapter 370.

Prognosis

Disability affects 75% of stroke survivors enough to decrease their employability. Stroke can affect people physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion. Dysfunctions correspond to areas in the brain that have been damaged.

Some of the physical disabilities that can result from stroke include muscle weakness, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, speech loss, vision loss and pain. If the stroke is severe enough, or in a certain location such as parts of the brainstem, coma or death can result.

Emotional problems following a stroke can be due to direct damage to emotional centers in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety, panic attacks, flat affect (failure to express emotions), mania, apathy and psychosis. Other difficulties may include a decreased ability to communicate emotions through facial expression, body language and voice.

Wade S. Smith, S. Claiborne Johnston, J Donald Easton. Cerebrovascular Disease. Harrison : The Principles of Internal Medicine vol.4. Chapter 370.

Preventions

-Body weight management

-Lipid fraction management

-Healthy lifestyle and exercise

-Diet management

Wade S. Smith, S. Claiborne Johnston, J Donald Easton. Cerebrovascular Disease. Harrison : The Principles of Internal Medicine vol.4. Chapter 370.

38

HEMORRAGIC STROKE

DDSTROKE HEMORAGICDefinitionStroke or injure the cerebrovaskuler is brain function loss resulted by desisting it blood supply to brain shares often this iskulminasi of disease serebrovaskuler for a number of yearsEtiologyThrombosis ( dilution clot in brain vein ) Cerebral embolism ( clot of other;dissimilar material or blood ) Iskemia ( Degradation of blood stream to brain area)PatomekanismeBrain embolism result the blood stream to brain decrease or desisted is at all to area of distal brain so that brain of insuffiency of source of calorie of berpa of other;dissimilar mineral and glucose and also oxygen Clinical symptomParalisis at adversative side foot/feet, balance trouble, cognate trouble, trouble sensori, afasia, memory damage, dll Therapycontrol of Sugar of blood and blood pressure, diuretik, antokoaulan, antitrombosit, Endosteroktomi Karotis, Revaskularisasi, konseling psikososial

40

TUMOR INTRACRANIAL

Definition

Brain tumours are among the most devastating of all malignant disease, frequently producing profound and progressive disability leading to death. Simplified classification of brain tumours:

1. Primary tumours: gliomas, astrocytoma, glioblastoma multiforme, ependyoma, oligodendrodlioma, etc.

2. Secondary tumours: common sites of origin, lung, breast, melanoma, etc.

Etiology

Very little is known of the etiology:

1. Several familial syndromes

2. Cranial radiation

Epidemiology

Brain tumours are slightly more common in males (1,2:1), with the exception of meningiomas, which are commoner in women.

Clinical Features

Symptoms can be divided into the following groups:

1. The tumour can exert a mass affect and lead to raised intracranial pressure, with headache, drowsiness, nausea and vomiting as the cardinal symptoms

2. There is a large group of focal symptoms caused by damage to local structures

3. The third group of symptoms results from remote endocrine effects, occurring with tumours of the pituitary and hypothalamus

4. Tumours of the CNS occasionally metastasize

5. Childhood brain tumours may present with other symptoms including weight loss, precocious puberty, growth failure and macrocephaly in addition to the classical symptoms noted in tumours of adults

Supporting Examination

CT and MRI

Management

Surgical removal or biopsy is desirable both for histological diagnosis and sometimes for definitive treatment

Prognosis

Malignant gliomas, the prognosis is heavily dependent on tumour grade and on other well-established prognostic factors. Patients with malignant glioma fall chiefly into two prognostic groups since those with grade I and II tumours have a relatively good prognosis and 5 and 10 year survival rates of approximately 65 and 35%, whereas those with grade III and IV tumours have a 5 year survival rate of under 10%, with a much worse prognosis in the grade IV category.

Medulloblastoma, age at diagnosis and completeness of excision are both important; children over 15 years of age have a better prognosis.

Ependyoma, prognosis depends on tumour grade. The median survival following surgery in low-grade ependyoma is approximately 10 years. Recurrences are frequently of a higher histological grade, and median overall survival in high-grade ependyoma is no better than 2-3 years.

Pituitary tumours and meningiomas, have an excellent prognosis following surgical removal and, where appropriate, postoperative radiotherapy

7. What are the treatments given to the patient?

Acute Stroke in Emergency Unit

Stabilize the airway, breathing, and circulation.

Give an intubation if the patient have a stupor or breath failure.

Stabilize patients fluid with NaCl 0,9% IV 20 ml/ hour, dont give a hypotonic fluid (Dextrose 0,9%, NaCl 0,45%, etc) because it can make a meaningful progress for their brain edem.

Oxygenation for 2 4 l/ minute

Give a NGT action.

Ask to get an ECG test and thorax rontgen

Get a Blood examination

Get an alcohol examination, hepar function test, Blood gas, toxicology screening if theres some indications.

Continue by history taking and physical examination.

And for gold standard: CT Scan or Magnetic Resonantion.

Manshoer, Arif. 2001. Kapita Selekta Kedokteran edisi 3 jilid 2. Jakarta.

Non Hemorragic Stroke

Trombolizes with rtPA (Recombinant Tissue- Plasminogen Activator) within 3 hours if the result of CT Scan is normal.

Do the therapy in therapy windows for 27 hours to decrease the risk progression or neurology deterioration.

Neurology deterioration includes to:

For the edem cause of infarc, we give a hypertonic or isotonic fluid.

For Infarc territorial extension, we optamilize a volume status and blood tension.

For the hemorragic conversion, we give an anti coagulanodepend on the risk of patient.

Prevent an early repeating stroke ( at least more than 30 days after the first onset).

Manshoer, Arif. 2001. Kapita Selekta Kedokteran edisi 3 jilid 2. Jakarta.

Hemorragic Stroke

If the protrombin result is longer, give FFP and Vitamin K till get a normal numbers.

Control the blood tension.

Get an angiography.

Consule to The Spesialist of Nerve Surgery.

Give a mannitol 20% for patient in comateus.

Give Fenitoin if theres a wide bleeding and low consciousness.

Give a hipervolemic fluid and nifodipin to prevent a vasospasme.

Manshoer, Arif. 2001. Kapita Selekta Kedokteran edisi 3 jilid 2. Jakarta.

8. How to prevent this disease?

Primary:

National campaign

Free and Health life style withour stroke

Secondary:

Modifice a risk life style.

Family support

Medica mentosa

Invasif action: flebotomi for polysutemia, enarterectomy, etc

Manshoer, Arif. 2001. Kapita Selekta Kedokteran edisi 3 jilid 2. Jakarta.

9. What are the risc factors related by this case?

STROKE RISK FACTOR

1. Stroke risk factors can not be modified

- Age

- Gender

- Ethnic

- Family History

(Reference: http://eprints.undip.ac.id/33923/3/Bab_2.pdf )

2. Stroke risk factors can be modified

- Risk factors (have been proven):

a. Hypertension

b. General fibrillation

c. Smoking

d. Diabetes

(Reference: http://eprints.undip.ac.id/33923/3/Bab_2.pdf )

Cont..

e. Hyperlipidemia

f. Carotid stenosis

g. A cursory history of ischemic attacks

h. Obesity

i. Sickle cells disease

(Reference: http://eprints.undip.ac.id/33923/3/Bab_2.pdf )

- Risk factors (have not been proven):

a. Heart disease

Myocard infarction

Left ventrivuly dysfunction

Heart valve disease

Left ventrivuly hypertrophy

Septurm atrium aneurysm

Mitral anuler calsification

(Reference: http://eprints.undip.ac.id/33923/3/Bab_2.pdf )

Cont..

b. Mitral valve rupture

c. Ateroma arcus aorta

d. Poor diet style

e. Lipoprotein

f. Alcohol consumption

g. Oral contraception

h. Druge abuse

i. Hyperfibrinogemia

j. Migrain

(Reference: http://eprints.undip.ac.id/33923/3/Bab_2.pdf )

3. Infection / chronic inflammation

(Reference: http://eprints.undip.ac.id/33923/3/Bab_2.pdf )

10. What is the Islamic perspective related to this case?

ISLAMIC PERSPECTIVE

Prophet said:

We are type of person that eat before hungry, and if we eat, we dont eat too much

Sujoods benefit:

If we do the sujood in the right way, we will get many benefits

When our heart position on upper side of our brain, it will cause our blood that full of oxygen will flow more to our brain.

SUMMARY

Our group takes a summary of this case is suspect Non Hemorragic Stroke. It looks from the sudden symtomps and patients history. But we still need to do some gold standard for this patient such as CT Scan, MRI, etc.

DAFTAR PUSTAKA

Greenstein, Ben. Dkk. 2010. At a Glance Sistem Endokrin. Edisi Kedua.Jakarta: Erlangga Medical Series. Halaman 8-9.

Price, Sylvia. Patofisiologi jilid 2. EGC. Jakarta

Buku Ajar IlmuPenyakitDalam. Jilid 3 Edisi 5.Halaman 1998]

McPhee SJ, Lingappa V, Ganong WF. Pathophysiology of Disease. An introduction to clinical medicine. 4th ed, New York: Lange Medical Books/McGraw Hill, 2003 p 556-76.

Weetman AP. Graves Disease. N Engl J Med 2000; 343: 1236-41.

Royani, Ida. Penuntun CSL Sistem Endokrin 2015. FK UMI

McGlynn, Burnside. Adams Diagnosis Fisis edisi 17. EGC. Jakarta

Tandra, Hans. Mencegah dan Mengatasi Penyakit Tiroid. EGC. Jakarta

Buku Ajar Ilmu Penyakit Dalam, halaman 2003-2005

Panduan Praktik Klinis Bagi Dokter di Fasilitas Pelayanan Kesehatan Primer. Menteri Kesehatan RI no.5 tahun 2014. Jakarta

Ilmu Penyakit Dalam. Edisi v. Jilid III. Hal 2720

Thank you..^^