Cases of Neuropathy
INTRODUCTION
Peripheral neuropathy describes
damage to the peripheral nervous
system.
More than 100 types of peripheral
neuropathy have been identified,
Impaired function and symptoms depend
on the type of nerves that are damaged:
motor, sensory, or autonomic
INTRODUCTION
Motor nerves
Sensory nerves
Autonomic nerves
SARAF PERIFER
Epidemiology
Prevalence of peripheral neuropathy in the
family medicine :
Person older in 55 years old 8%
General population 2,4 % .
Type 2 Diabetes Melitus 26,4 %
EPIDEMIOLOGY
The incidence of peripheral neuropathy is not
known, but it is a common feature of many
systemic diseases.
Diabetes and alcoholism are the most
common etiologies of peripheral neuropathy
The primary worldwide cause of treatable
neuropathy is leprosy.
Neuropathies associated with human
immunodeficiency virus (HIV) infection
account for an increasing number of cases.
EPIDEMIOLOGY
Peripheral neuropathy has numerous
other causes, including hereditary, toxic,
metabolic, infectious, inflammatory,
ischemic and paraneoplastic disorders.
The number of peripheral neuropathies for
which an etiology cannot be found despite
extensive evaluation ranges from 13 to 22
percent.
CLASSIFICATION OF PERIPHERAL
NEUROPATHY
1. According to the number of nerves :
Associations
Systemic diseases
Metabolic disorders
Exogenous toxins
CLASSIFICATION OF PERIPHERAL
NEUROPATHY
2. ACCORDING TO THE TYPE OF FIBER
Motor fibers: necessary for all our voluntary or intentional
movements, such as walking, stretching, or making a
fist; motor neuropathies may result in weakness or
spasms.
Sensory fibers: involved with feeling and touching;
sensory neuropathies cause abnormal sensations such
as pain, cold, heat or burning sensations, tingling, or
numbness.
Autonomic fibers: concerned with involuntary functions.
autonomic neuropathies can cause changes in these
functions and include decreased perspiration, bowel and
bladder
CLASSIFICATION OF PERIPHERAL
NEUROPATHY
3. According to the pathology
Axonal Neuropathy
Demyelinating Neuropathy
4. According to the onset
Acute Neuropathy : eg trauma
Subacute Neuropthy : eg: GBS
Chronic Neuropathy
POSITIVE SYMPTOMS
Motor
Myokimia
Fasciculation
Dystonia
Sensory
Paraesthesia
Dysesthesia
Allodynia
Hyperaesthesia
Pain
Photopsia
Tinnitus
Autonomic
Vasoconstriction
Hyperhydrosis
Piloerection
History
Physical Examination
EDX studies
Epidermal skin fiber density
Nerve biopsy
History
Neuropathy may present with variety of sign and
symptom s may be clasified negative or positive
Motor Symptoms
Positive symptoms: Kram,twiching,myokymia .
Negative symptoms: Weakness,fasting,fatigue.
Weakness may not be apreciated until 50%80% nerve lost.
Positive symptoms may present earlier in the
disease
Sensory Symptoms
Positive symptoms:burning or lansinating
pain,buzzing, allodynia, hiperalgesia,
tingling/parestesia.
Negative symptoms:hypestesia,gait
abnormalities ataxia, difficulty
differentiating hot and cold,and worsening
balance.
History
Impairment in activities of daily living
Detail regarding diseases onset ,duration
and progresion .
Any other patients with similar neurology
disorder.
Impairment of consciousness,visual
disturbances.
Social history :occupation,sexual
history,drug abuse ,alcohol,smoking.
History
Illness associated with neuropathy:
Diabetes Melitus, Hypothyroidism, Renal
insuffisiency, hepatic dysfuntion.
Patient with cancer: nutritional deficiency,
chemotheraphy side effect, paraneoplastic
syndrome.
Surgical: multiple orthopedic procedur .
Medication :HIV,Antibiotic,chemotheraphy.
Physical Examination
Gait: Tandem,toe/heel walk,hop,squat
Skeletal deformation :pes cavus,hammertoes, and
kyphoscoliosis are sugestive inherited
polineuropathy.claw hand is ulnar palsies.
Nerve elargemenet: infection (leprtosy),neoplasia
(neurofibromatosis)
Skin lesion: vasculitis rash,hipopigmentasi,
hiperpigmentasi,(poems diseases) oral ulcer (Behcet
disease,HIV)
Gum lesion: lead leines
Nail lesion: arsenic Thalium poisoning
Hair lesion: alopecia( hypothyroidism),curly.(giant
axonal neuropthy)
Physical Examination
Motor sign :
Negative : weakness,atrophy. weakness of flexion
and extension of the small toes and weaknes of
great toe extension may be early sign .
Positive :tremor,faciculation,myokimia,cramps
Cranial nerve assessment should include anosmia
(refsum disease,Vitamin B 12,deficiency),
Imparied ocular motility (botulism,Miller fisher),
Fascial weakness (GBS) .
Diagnostic Testing
Laboratory and genetic testing
Electrodiagnostic testing
Neurophysiologic testing (Evoked
potensial,TMS)
Quantitative Sensory testing
Autonomic testing
Nerve and skin biopsy
Imaging test.
Tests
Clinical disorders
Routine
Tests
Clinical disorders
Demyelinating neuropathy
Comprehensive metabolic
panel
Erythrocyte sedimentation
rate
Angiotensin-converting enzyme
levels
Sarcoidosis
Vasculitis
Thyroid-stimulating
hormone level
level
Vitamin B12
If indicated by clinical
suspicion
Glucose tolerance test, A1C
level
Diabetes mellitus
HIV antibodies
HIV
Hepatic panel
Liver disorders
Lyme antibodies
Lyme disease
Syphilis
Underlying malignancy
Antimyelin-associated
glycoprotein and
antiganglioside antibodies
Sensorimotor neuropathy
Antisulfatide antibodies
Autoimmune polyneuropathy
Cryoglobulins
Cryoglobulinemia
Sjgren syndrome
Genetic testing
Hereditary neuropathy
Electrodiagnostic studies
Electrodiagnostic studies are helpful in
determining the locatuion of peripheral
nervous system involment.
Magnetic stimulation and somatosensory
evoked potentials may assist in identifying
root plexus and proximal nerve.
Treatment
Treatment of peripheral neuropathy has two
goal :
Controling the underlying disease process
Treating trouble some symptom
Summary
History and physical examination remain
the most useful for tools for diagnostic
perpheral neuropathy
Characteristic of a neuropathy aids in
limiting the differential diagnoses and
includes temporal profile,hereditery,and
anatomic clasification
Determining wich diagnostic test evaluate
neuropathy is challenging
ETIOLOGI
Gerakan berulang-ulang pada pergelangan tangan
Gangguan endokrin
Idiopatik
GEJALA
Perasaan baal dan semutan pada tiga jari tangan
dimana keluhan ini meningkat di malam hari
sehingga pasien terbangun. keluhan berkurang
dengan mengibaskan tangan.
Nyeri dan baal bila menyetir, mengangkat tangan,
membaca koran.
Otot thenar menjadi lembek dan atrofi
Kelemahan terutama pada tangan kanan.
DIAGNOSTIC TEST
Tinels sign
Phalens sign
PEMERIKSAAN PENUNJANG :
1. Pemeriksaan KHS motorik dan sensorik
N. medianus
2. EMG
abductor pelicis brevis, flexor pollicis longus,
pronator teres, biceps dan triceps.
PENGOBATAN :
1. Kortiko steroid injeksi pada ligamentum di daerah
volar
2. Hindari gerakan berulang pada tangan,
Immobilisasi, splint
3. Operasi
DEMENSIA
DEFINISI
Sindroma penurunan kemampuan intektual progresif
yang menyebabkan kemunduran fungsi kognisi dan
fungsional, sehingga mengakibatkan gangguan
fungsi sosial, pekerjaan dan aktifitas sehari-hari.
JENIS DEMENSIA
1. Demensia vaskuler
2. Alzheimer
DEMENSIA VASKULER
DEFINISI :
Demensia yang disebabkan oleh gangguan
serebrovaskuler dengan penurunan kognisi mulai dari
ringan sampai berat.
GEJALA KLINIS
Gangguan perilaku dan psikis : depresi,
perubahan kepribadian, emosi labil, retardasi
psikomotor
disartria, disfagi, gejala ekstrapyramidal
gangguan keseimbangan, sering jatuh
gangguan berjalan
gangguan miksi
PEMERIKSAAN PENUNJANG
Darah : hematologi, faktor risiko stroke
CT Scan kepala
MRI
Tes Neuropsikologi : MMSE, CDT, ADL,
Skala depresi geriatrik
PENGOBATAN FARMAKOLOGI
a. Untuk gangguan kognisi
- Donepezil HCL 5 mg 1 x 1 tab
- Rivastigmin
- Galantamin
b. Untuk gangguan perilaku
Untuk depresi : antidepresan
Untuk halusinasi :
- Haldol 1 x 0,5-2 mg/hari
- Risperidon tablet 1 x 0,5-2 mg/hari