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Plenary Discussio

1.AINIL

2.DEBBY MULYA RAHMY

3.ENDAH SETYANINGSIH

4.MARWAH NISA HIDAYAT

5.MAYANG MALIANI

6.MUHAMMAD

BINTANG ILH

7.NIDIANTI NE

8.NILA PEBRY

9.SRI MARDLA

10 B - 01/09/1

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SCENARIO : PainMrs. Nani, 40 years old go to the doctor with pain in the right wrist, especially at nigh

months ago. Initially just tingling, numbness or a sense of feeling like electric shock on finger 14 and a half fingers right hand, though sometimes felt about the whole finger. These complaiusually more prominent at night. Other Symptoms of pain in the right hand is perceived more senight so she often woke up. The pain is generally diminished when she massage or domovement or placing a hand on a higher position. Pain will also be reduced when she rested her h

From examination: thenar muscle atrophy, Phalen Test (+), and Tinel Test (+). Mrs.Nani

medication and it is recommended to reduce the movement of his right wrist. He asked the dothese drugs can be taken together with drug for headache?

From history known since last year Mrs. Nani often experience headaches pulsating,accompanied by nausea and sometimes vomiting, often accompanied by photophobia and sonHeadache attack can last up to four hours, even up to three days so that she does not come to wor

As a medical student, how do you explain Mrs.Nani disease?

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Terminology

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Formulate and Analy1. Why Mrs. Nani felt pain in the right wrist, especially at night since 3 months ago?

Is there a correlation between age and gender with Mrs. Nani conditions?

● Pain in the wrist and thumb can be caused by injury or inflammation in the soft tissue joints.

● The pain in the wrist can arise because of the pressure on the medianus nerve innervate the palm of the hand and fingers.

● There is a relationship between age and gender with Mrs. Nani condition that the range was 30-60 years and male : female = 1: 3

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1. Plan Your Time2. Identify Active and Reactive

2. Why is initially just tingling, numbness or a sense of feeling like electric shock on fin1,2,3, and 4 and a half fingers right hand?

● Feel numbness and tingling is usually caused by depressed n. medianus. The pressuusually caused by a thickening of the flexor retinaculum. At first the pressure only ca

numbness and tingling in the fingers 1,2,3, and 4 and a half fingers if it is too longemphasis can be on all the fingers, wrist, forearm and upper arm.

3. Why Mrs. Nani feel pain in the right hand, especially at night?● Because temperature is one of the stimulus from the onset of pain.

4. Why pain is reduced when a hand massage, moved, or placed in a higher position, an

when the hand is rested?● Repeated stress causes elevation of intravascular pressure as a result of venous blo

flow slows down. By doing massage, movement, or put in a higher position will impblood flow temporarily.

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5. How the interpretation of the examination?● Thenar muscle atrophy may be caused by disuse.● Phalen's test (+) and Tinel test (+) à Carpal tunnel syndrome

6. What medications are given and why it is recommended to reduce the movement of t

right wrist?● Analgesic medication● It is advisable to reduce wrist movement to relieve pain, if still driven the components

the carpal tunnel will fluctuate causing pain.

7. Why since one year ago Mrs. Nani often headache, pulsating, moving, nausea and

vomiting, accompanied by photophobia and sonofobia?● Migraine headaches à interruption of blood flow● Nausea and vomiting àcaused by stimulation specific receptors●

Sonofobia and fotofobiaà due to hypersensitivity

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SCHEME

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Learning Objec

1. Mechanism of Pain2. Headache3. Diseases of Peripheral Ner4. Degeneration and Regener

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1. Mechanism o

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The perception of a noxious stimulus thatin the dorsal horn and involves the entirecord and brain.

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Typ1. Quick pain:

● 0.1 s after stimulus● A-delta type of myelinated nerve fibers● Acute pain, sharp

2. Slow pain :● 1 s - few minutes after stimulus● Type C nerve fibers are not myelinated● Chronic Pain

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Afferent pathways• From nociceptors , transmitted by small A-delta fibers and C- fibers to thesynapses with neurons in the dorsal horn .

• From dorsal horn transmitted to higher parts of the spinal cord and to the rest of theby spinothalamic tracts .

Efferent analgesic systemIts role: Inhibition of afferent pain signalsMechanisms: Pain afferents stimulates the neurons in Periaqueductal Gray

matter surrounding the cerebral aqueduct in the midbrain results in activat

(descendent) anti-nociceptive pathways. From there the impulses are trans

the spinal cord to the dorsal horn - inhibit or block transmission of nociceptive.

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The role of the spinal● Most afferent pain fibers terminate in the dorsal horn of the spinal segm

enter. Some, however, extend toward the head or the foot for several segments b

terminating● The A fibers, some large A-delta fibers and small C- fibers terminate in

dorsal horn and in the substantia gelatinosa● The laminae than transmit specific information (about burned or crushed skin

gentle pressure) to 2nd afferent neuron.●

2nd

afferent neurons transmit the impulse from the s ubstantia gelatilaminae through the ventral and lateral horn , crossing in the same or asegment , to the other side of the cord. From there the impulse is carried throspinothalamic tract to the brain . The two divisions of spinothalamic tract are ka. Neo -spinothalamic Tractb. Paleo -spinothalamic Tract

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2. Headaches

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Causes o1. Traction or dilatation of intracranial or extracranial ar2. Traction of large extracranial veins3. Compression, traction or inflammation of cranial an

nerves4. Spasm and trauma to cranial and cervical muscles.5. Meningeal irritation and raised intracranial pressur6. Disturbance of intracerebral serotonergic projections.

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MPathophysiology:

● Cortical spreading depression activates the trigeminal and parasympathewhich causes vasodilatation and release of neuropeptides that cause in

● Serotonin 5 HT receptors modulate the release of neurogenic peptides.

5 Attacks of Migraine:●

Headache lasting 4-72 hours.● Must be associated with nausea or vomiting or photophobia and phonopho● Must have 2 of the following:

1. Unilateral2. Pulsating3. Moderately severe.4. Aggravated by physical activity

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Causes of Tension-type Headache● Some evidence that like migraine caused by serotonin imbalance but to

than migraine.● This would indicate that similar treatments would work.

Episodic Tension-type Headche● Tension type headaches < 15 per month .

● Lasts 30 mins to 7 days●

No nausea or vomiting● No photophobia and phonophobia (1 ok)● Headache has at least 2 of the following criteria:

1) Pressing/tightening2) Bilateral3) Mild-moderate4) Not aggravated by physical activity.

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Treatment of Tension-type Headache● Simple analgesia : Ibuprofen is more effective than Acetaminophen.● Combine analgesics with a sedating anit-histamine (eg: diphenhy● Limit treatment to 2 days a week to prevent rebound headaches.

Chronic Tension-type Headache● Develops from episodic tension type headaches●

Familial tendency.● Affect women more than men● Most common in middle age● Stress is often a trigger● Average duration is 4-13 hours .

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Treatment of Chronic Tension-type Hea ● Treating each headache increases the frequency and severity of the heada● Reserve medications for worse than usual headache.● Expert opinion: treat 2 headaches a week.

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ClusA. At least 5 attacks fulfilling criteria B-DB. Severe or very severe unilateral orbital, supraorbital and/or temporal

lasting 15-180 minutes if untreatedC. Headache is accompanied by 1 of the following:

1. Ipsilateral conjunctival injection and/or lacrimation2. Ipsilateral nasal congestion and/or rhinorrhoea3. Ipsilateral eyelid oedema4. Ipsilateral forehead and facial sweating5. Ipsilateral miosis and/or ptosis6. A sense of restlessness or agitation

D. Attacks have a frequency from 1/2 day to 8/day

E. Not attributed to another disorder

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Episodic Cluster HeadacheA. Attacks fulfilling criteria A-E for the criteria of the previous slide:

headache.

B. At least two cluster periods lasting 7-365 days and separated by pain-fremission periods of 1 month.

Chronic cluster headacheA. Attacks fulfilling criteria A-E for the criteria of the previous slide:

headache.

B. B. Attacks recur over >1 year without remission periods or with remisperiods lasting <1 month.

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3. Diseases of Peripher

B ll’ P l

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Bell’s PalsyIncindence:

The incidence of Bell palsy in the United States is appr23 cases per 100,000 persons.

Internsationally: The incidence is the same as in thStates.

Pathopysiology:

● Main cause of Bell's palsy is latent herpes virsimplex virus type 1 and herpes zoster virus)reactivated from cranial nerve ganglia.

● Inflammation of the nerve initially results in neurapraxia,

● Herpes zoster virus shows more aggressiv

behaviour than herpes simplex virus type 1

h

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pathopy

● The palsy is often sudden in onset and evolves rapidly, with maximalweakness developing within two days.

● Associated symptoms may be hyperacusis, decreased production of tand altered taste.

● Patients may also mention otalgia or aural fullness and facretroauricular pain, which is typically mild and may precede the palsy.

● A slow onset progressive palsy with other cranial nerve deficheadache raises the possibility of a neoplasm

Ph

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Phy● Bell's palsy causes a peripheral lower motor neurone palsy,● which manifests as the unilateral impairment of movement in the faci

platysma muscles, drooping of the brow and corner of the mouth, and imclosure of the eye and mouth.

● Bell's phenomenon—upward diversion of the eye on attempted closure lid— is seen when eye closure is incomplete.

● Polyposis or granulations in the ear canal may suggest cholesteatoma or mal

otitis externa.● Vesicles in the conchal bowl, soft palate, or tongue suggest Ramsay Hunt

syndrome● The examination should exclude masses in the head and neck.● A deep lobe parotid tumour may only be identified clinically by careful

examination of the oropharynx and ipsilateral tonsil to rule out asymmetry.

D

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D● Bell palsy is a diagnosis of exclusion.● Other disease states or conditions that present with facial palsies are often

misdiagnosed as idiopathic.

M● The main aims of treatment in the acute phase of Bell's palsy are to speed re

and to prevent corneal complications.● Treatment should begin immediately to inhibit viral replication and the ef

subsequent pathophysiological processes that affect the facial nerve.● Psychological support is also essential, and for this reason patients may

regular follow up.

G ill i B S

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Guillain Barre Sy● is an acute inflammatory demyelinating polyneuropathy (AIDP). It is

triggered by an acute infectious process.● Etiology is unclear, but an autoimmune response is strongly suspected.● Approximately half of the people who develop Guillain- Barré syndrome have

febrile illness 2 to 3 weeks before the onset of symptoms.● The febrile infection is usually respiratory or gastrointestinal.● Approximately 25% of patients with this disease have antibodies to either

cytomegalovirus or Epstein-Barr virus.

Pa

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Pa● In Guillain-Barré syndrome, the myelin sheath surrounding the axon is lost.● Demyelination is a common response of neural tissue to many agents and co

including physical trauma, hypoxemia, toxic chemicals, vascular insuffic

immunological reactions.● Loss of the myelin sheath in Guillain-Barré syndrome makes nerve impulse trans

aborted

Clinic● The syndrome may develop rapidly over the course of hours or days, or may take u

4 weeks to develop.● Most patients demonstrate the greatest weakness in the first weeks of the disorder.● Patients are at their weakest point by the third week of the illness.● In the beginning, a flaccid, ascending paralysis develops quickly.● The patient is most commonly affected in a symmetrical pattern.

C inica Ma

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C inica Ma● The patient may first notice weakness in the lower extremities that may quickly extend to

weakness and abnormal sensations in the arms.● Deep tendon reflexes are usually lost, even in the earliest stages.● The trunk and cranial nerves may become involved.● Respiratory muscles can become affected, resulting in respiratory compromise.● Autonomic disturbances such as urinary retention and orthostatic hypotension may also o● Superficial and deep tendon reflexes may be lost.● Some patients experience tenderness and pain on deep pressure or movement of some musc● Sensory symptoms of paresthesias, including numbness and tingling, may occur.● Pain is a complaint in a large number of patients.● It is aching in nature and often compared with the feeling of muscles that have been overexe● If there is cranial nerve involvement, cranial nerve VII, the facial nerve, is most often affect● Guillain-Barré syndrome does not affect level of consciousness, pupillary function, o

function.● Symptoms may progress for several weeks. The level of paralysis may stop at any point.● Motor function returns in a descending fashion.● Dem elination occurs ra idl but the rate of rem elination is a roximatel 1 to 2 mm e

D

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D● The history of the onset of symptoms can be revealing because sympt

Guillain-Barré syndrome usually begin with weakness or paresthesias of thextremities and ascend in a symmetrical pattern.

● A lumbar puncture may be performed and reveal increased protein.● Also, nerve conduction studies record impulse transmission along the nerve fib● Pulmonary function tests are done when Guillain-Barré syndrome is suspe

establish a baseline for comparison as the disease progresses.● Declining pulmonary function capacity may indicate the need for

ventilation and management in an ICU.

Cli i l

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Clinical

● The first therapy proven to benefit patients with Guillainsyndrome is plasmapheresis.

● This procedure mechanically removes humoral factors.● Intravenous immunoglobulin (IVIG) is also useful in

Guillain-Barré syndrome.

M th i G

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Myasthenia Gis an autoimmune neuromuscular disease leading to fluctuating m

weakness and fatigability. It is an autoimmune disorder, inweakness is caused by circulating antibodies that block acetylreceptors at the post-synaptic neuromuscular junction, inhibitinstimulative effect of the neurotransmitter acetylcholine.

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● Myasthenia gravis is an autoimmune disorder.● The factors that trigger the autoimmune process are not known, b

thymus gland is involved.● The thymus lies behind the sternum and may extend down

diaphragm or up to the neck.● This gland plays a role in the responsiveness of T cells to foreign anti● The thymus gland is large in children and small in adults.● By adulthood, the gland has shrunken and has nearly been replaced b● Abnormalities in the thymus gland frequently occur in patien

myasthenia gravis.● Eighty percent of patients with myasthenia gravis have thymal hyperp

P th

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Patho● Myasthenia gravis is a result of circulating antibodies d

toward the skeletal muscle acetylcholine receptors.● This leads to a decrease in end plate depolarization, which m

insufficient to generate an action potential.● This results in a failure of the muscle to contract.

Clinical M

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Clinical M● The hallmark of myasthenia gravis is fatigability. Muscles become progressively we

periods of activity and improve after periods of rest. Muscles that control eye a

movement, facial expressions, chewing, talking, and swallowing are especially susceptib● The muscles that control breathing and neck and limb movements can also be affected● Symptoms, which vary in type and severity, may include asymmetrical ptosis (a droop

or both eyelids), diplopia (double vision) due to weakness of the muscles that cmovements, an unstable or waddling gait, weakness in arms, hands, fingers, legs, anchange in facial expression, dysphagia (difficulty in swallowing), shortness of dysarthria (impaired speech).

● In myasthenic crisis a paralysis of the respiratory muscles occurs, necessitatinventilation to sustain life. In patients whose respiratory muscles are already weak, crisetriggered by infection, fever, an adverse reaction to medication, or emotional stress. heart muscle is only regulated by the autonomic nervous system, it is generally unaffecte

D

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D● Patient’s history

● Patients may present with complaints of double vision or dreyelids.

● Also, myasthenia gravis causes weakness of the shouldermuscles.

● The cranial nerve examination may reveal ptosis and diplopia

● Motor weakness may be exhibited● Blood is drawn for acetylcholine receptor antibodies● Electromyography (EMG)

Clinicial

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● Use of medications to enhance neuromuscular transmission; sucanticholinesterases (Pyridostigmine (Mestinon), and st(Prednisone)

● Long-term immunosuppression with corticosteroids, azathio

(Imuran), cyclophosphamide (Cytoxan), or cyclosporine;● Short-term immunomodulation with plasmapheresis or IVI

thymectomy.

Clinicial

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4. DEGENERATION ANEURON

RESPONSE OF TH

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RESPONSE OF TH

● All neurons - despite different morphologies - react similarly● Principles -If cell body damaged, the neuron dies, and is not rep

by cell division in mature brain. If the axon is damaged or sevea distance from the soma, there is a good chance of regenera

primarily in the PNS.● CNS neurons have the capacity to regenerate.

REACTIONS TO INJUR

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REACTIONS TO INJURImmediately1. Synaptic transmission off2. Cut ends pull apart and seal up, and swell, due to axonal transport in both directionsHours later3.Synaptic terminal degenerates - accumulation of NF, vesicles.4.Astroglia suround terminal normally; after axotomy, interpose between terminal and and cause terminal to be pulled away from postsynaptic cell.

Days - Weeks

5. Myelin breaks up and leaves debris (myelin hard to break down).

6. Axon undergoes Wallerian degeneration

7. Chromatolysis - cell body swells; nissl and nucleus eccentric.

Neurons in the PNS ca

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Neurons in the PNS ca

a. After degeneration of distal axon and myelin, macrophages clean up debris.b. Macrophages release mitogens that induce Schwann cells to dividec. The myelin-forming Schwann cells repopulate the nerve sheaths;d. Schwann cells make laminine. Macrophages make interleukin, which induces Schwann cells to makeFactor.f. Axons sprout, and some sprouts enter new Schwann cell tubesg. Axonal growth cones successfully grow

Neurons in the CNS have a limited capa

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Neurons in the CNS have a limited caparegenera

● Growth is impeded by negative elements in the environment-extramatrix ( laminin ) is sparse; inhibitory proteoglycans incfactors have different distributions compared to young brain

● Intracellular growth elements such as GAP-43 (important fosignaling/growth cone advance) are low

● *Glial cells inhibit growthOligodendrocytes (CNS myelin) are the most inhibitoryAstrocytes accumulate in the scar around injury siteMacrophages also accumulate; role of microglia unclear

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Tha