After posting about the definition, etiology, and patofisiology, today Mbah Dukun Bagong, original shaman from Indonesia, will explain how to diagnose Guillain Barre Syndrome and how about prognosis.
SUPPORTING EXAMINATIONS
1. Laboratory tests
Laboratory picture shows elevation of protein levels in the cerebrospinal fluid (> 0.5 mg%) without being followed by the elevation of the number of cells in the cerebrospinal fluid, this is called cytoalbuminic dissociation. The elevation was started at 1-2 weeks of disease onset and reached its peak after 3-6 weeks. The number of mononuclear cells was <10 cells/mm3. However in a minority of patients found no elevation of protein levels in cerebrospinal fluid. There is may increasing serum immunoglobulin. Some patients, can occur with hyponatremia caused by SIADH (syndrome Inapproriate antidiuretic hormone).
2. Electrophysiological examination (EMG)
Electrodiagnostic manifestations that supports to diagnosis is the slowing speed of motor and sensory nerve delivery. Retention of elongated distal motor speed slows down delivery of f-wave, indicating a slowdown in the proximal segments and nerve roots. In addition to supporting the diagnosis of electrophysiological examination is also useful for determining the prognosis of the disease: if found potential denervation suggests that the longer the healing of disease and did not recover completely.
DIAGNOSIS
Commonly used diagnostic criteria are the criteria of the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS), namely:
1. The characteristics necessary for diagnosis:
The occurrence of progressive weakness Hyporeflexia
2. The characteristics that strongly support the diagnosis of GBS:
a. Clinical symptoms:
Diagnosis of GBS is clinically mainly enforced. GBS is characterized by an acute paralysis / weakness of motor progresive rapidly (maximal within 4 weeks, 50% reached the peak in 2 weeks, 80% in 3 weeks, and 90% in 4 weeks), relatively symmetrical with loss of tendon reflexes (areflexi or hipoflexia) and preceded by paresthesias of two or three weeks after suffering a fever accompanied by dissociation cytoalbumine on liquor and mild sensory disturbances and motor peripheral. Symptoms of cranial nerves ± 50% occurred N VII parese and often bilateral. Other brain nerves which supply can be affected especially the tongue and muscles of swallowing, sometimes <5% of cases, starting from the muscle ekstraocculer neuropathy or other brain nerves. Recovery: starts 2-4 weeks after progression stops, can be elongated up to several months. Autonomic dysfunction. Tachycardia and arrhythmia, postural hypotension, hypertension, and vasomotor symptoms. No fever at onset of neurological symptoms.
b. The characteristics of cerebrospinal fluid abnormalities are strongly supporting the diagnosis:
Cerebrospinal fluid protein picture of the CSS. Increased after 1 week of symptoms or an increase in LP serial number of cerebrospinal fluid mononuclear cells <10 cells / mm.
Variants:
1) No increase in protein after 1 week of symptom CSS
2) The number of cells CSS: 11-50 MN/mm3
c. EMG examination
Electrodiagnostic picture that supports the diagnosis: there is a slowdown in the speed of conductivity / nerve conduction block on EMG even in 80% of cases. Usually the speed of carrying about 60% of normal.
DIFFERENTIAL DIAGNOSIS
1. Asymmetric paralysis that persisted.
2. Bladder and bowel disorders are settled.
3. Bladder and bowel disturbances at onset.
4. The number of mononuclear cells in cerebrospinal fluid> 50 cells mm3.
5. There PMN leukocytes in the cerebrospinal fluid.
6. Impaired sensibility demarcated.
7. Poliomyelitis, botulism, hysteria or toxic neuropathies (eg due to lead poisoning / lead, itrofurantoin, dapsone, organophosphates), Diphtheric paralysis, miller-fisher syndrome, cranial sensory deficit, Pandisautonomia pure, Chronic demyyelinative acquired neuropathy, acute intermittent Porphyria.
Prognosis
Before the existence of artificial ventilation approximately 20% of patients died due to respiratory failure. Today's death ranged from 2-10%, with cause of death due to respiratory failure, impaired autonomic function, pulmonary infection and pulmonary embolism. Most patients (60-80%) recover completely within six months. A small percentage (7-22%) healed within 12 months with mild motor abnormalities and atrophy of the small muscles in the arms and leg. 3-5% of patients relapse.
1. Laboratory tests
Laboratory picture shows elevation of protein levels in the cerebrospinal fluid (> 0.5 mg%) without being followed by the elevation of the number of cells in the cerebrospinal fluid, this is called cytoalbuminic dissociation. The elevation was started at 1-2 weeks of disease onset and reached its peak after 3-6 weeks. The number of mononuclear cells was <10 cells/mm3. However in a minority of patients found no elevation of protein levels in cerebrospinal fluid. There is may increasing serum immunoglobulin. Some patients, can occur with hyponatremia caused by SIADH (syndrome Inapproriate antidiuretic hormone).
2. Electrophysiological examination (EMG)
Electrodiagnostic manifestations that supports to diagnosis is the slowing speed of motor and sensory nerve delivery. Retention of elongated distal motor speed slows down delivery of f-wave, indicating a slowdown in the proximal segments and nerve roots. In addition to supporting the diagnosis of electrophysiological examination is also useful for determining the prognosis of the disease: if found potential denervation suggests that the longer the healing of disease and did not recover completely.
DIAGNOSIS
Commonly used diagnostic criteria are the criteria of the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS), namely:
1. The characteristics necessary for diagnosis:
The occurrence of progressive weakness Hyporeflexia
2. The characteristics that strongly support the diagnosis of GBS:
a. Clinical symptoms:
Diagnosis of GBS is clinically mainly enforced. GBS is characterized by an acute paralysis / weakness of motor progresive rapidly (maximal within 4 weeks, 50% reached the peak in 2 weeks, 80% in 3 weeks, and 90% in 4 weeks), relatively symmetrical with loss of tendon reflexes (areflexi or hipoflexia) and preceded by paresthesias of two or three weeks after suffering a fever accompanied by dissociation cytoalbumine on liquor and mild sensory disturbances and motor peripheral. Symptoms of cranial nerves ± 50% occurred N VII parese and often bilateral. Other brain nerves which supply can be affected especially the tongue and muscles of swallowing, sometimes <5% of cases, starting from the muscle ekstraocculer neuropathy or other brain nerves. Recovery: starts 2-4 weeks after progression stops, can be elongated up to several months. Autonomic dysfunction. Tachycardia and arrhythmia, postural hypotension, hypertension, and vasomotor symptoms. No fever at onset of neurological symptoms.
b. The characteristics of cerebrospinal fluid abnormalities are strongly supporting the diagnosis:
Cerebrospinal fluid protein picture of the CSS. Increased after 1 week of symptoms or an increase in LP serial number of cerebrospinal fluid mononuclear cells <10 cells / mm.
Variants:
1) No increase in protein after 1 week of symptom CSS
2) The number of cells CSS: 11-50 MN/mm3
c. EMG examination
Electrodiagnostic picture that supports the diagnosis: there is a slowdown in the speed of conductivity / nerve conduction block on EMG even in 80% of cases. Usually the speed of carrying about 60% of normal.
DIFFERENTIAL DIAGNOSIS
1. Asymmetric paralysis that persisted.
2. Bladder and bowel disorders are settled.
3. Bladder and bowel disturbances at onset.
4. The number of mononuclear cells in cerebrospinal fluid> 50 cells mm3.
5. There PMN leukocytes in the cerebrospinal fluid.
6. Impaired sensibility demarcated.
7. Poliomyelitis, botulism, hysteria or toxic neuropathies (eg due to lead poisoning / lead, itrofurantoin, dapsone, organophosphates), Diphtheric paralysis, miller-fisher syndrome, cranial sensory deficit, Pandisautonomia pure, Chronic demyyelinative acquired neuropathy, acute intermittent Porphyria.
Prognosis
Before the existence of artificial ventilation approximately 20% of patients died due to respiratory failure. Today's death ranged from 2-10%, with cause of death due to respiratory failure, impaired autonomic function, pulmonary infection and pulmonary embolism. Most patients (60-80%) recover completely within six months. A small percentage (7-22%) healed within 12 months with mild motor abnormalities and atrophy of the small muscles in the arms and leg. 3-5% of patients relapse.
