تشخیص

Differential Diagnosis of acute flccid paralysis

  Brain lesions

 n  Brain bilateral strokes

 n  Acute cerebellar ataxia syndrome.

 n  Posterior fossa structural lesions.

 n  Brainstem strokes.

 n  Brainstem encephalitis.

  Acute myelopathy

 n  Space-occupying lesions.

 n  Acute transverse myelitis.

 n  Poliomyelitis.

Acute transverse myelitis

  n   sudden onset

  n   rapidly progressive

  n   Usually weakness of the lower extremities,

  n  The weakness is initially flaccid, but later it evolves into a spastic   paresis with uppermotor neuron signs

  n   loss of sensation

          A sensory level can be found in almost all

  n   sphincter control.

          Abnormal rectal tone is a frequent finding

    CSF:

  n  Abnormalities are found in more than half of patients and include   moderate lymphocytic pleocytosis and high protein level

  EMG-NCV:

  n  peripheral nerve conduction velocity is normal.

  n   compound muscle action potential amplitudes may be affected if   segmental anterior-horn cells are affected.

  n   Missing F waves or prolonged F latencies.

    MRI:

  n  relatively variable and nonspecific in ATM.

  n  spinal cord swelIing, longitudinal fusiform-like diffuse hyperintensities   on T2-weighted images,

  n  The value of MRI is to exclude other conditions that cause paraparesis.

Poliomyelitis

 n  The presenting symptom of paralytic poliomyelitis is

 n  Pain of the lower back.

 n  drowsiness, or irritability.

 n  Muscular pain, fasciculation,

 n  The fever that generally accompanies the paralysis .

 n  The paralysis appears during the first or second day of the major illness.

 n  Often it reaches maximum within a few hours.

  n   Spinal paralytic poliomyelitis is characterized by :

  n   an asymmetric.

  n    flaccid paralysis

  n   that more frequently involves the lower extremities.

  n   weakness is accompanied by muscle tenderness and spasm.

  n    Deep tendon reflexes in the affected area are usually absent.

  n   Autonomic involvement can be manifested by excessive sweating and    vasomotor disturbances.

  n   Some 10% to 20% of patients have bladder involvement,

  n   Sensory involvement are extremely rare.

    CSF:

  n  Abnormalities are found in more than half of patients and include   moderate lymphocytic pleocytosis and high protein level

  n  The virus is best isolated from the stool and oropharynx.

  n  Poliovirus has been isolated from the stool as early  as 19 days before   onset of illness and as late as 3 months after onset.

Peripheral neuropathy

 n  Guillain-Barre syndrome.

 n  Diphtheric neuropathy.

 n  Heavy metals, biological toxins or drug intoxication.

 n  Acute intermittent porphyria.

 n  Critical illness neuropathy.

  Guillain-Barre syndrome

 n  The paralysis usually begins in the lower extremities, then ascends

 n  Characteristically, it is symmetric.

        (in 9% asymmetric)

  v  minor differences between the sides are not rare.

  n   in approximately 15%, the proximal musculature is more extensively     involved.

  n   The deep tendon reflexes are generally absent,

          although increased reflexes and extensorplantar responses are occasionally   recorded during the initial days of the illness

  n   Cranial nerve palsies can appear(The facial nerve is most commonly      affected).

  n   Paralysis of the respiratory muscles is a common complication in severely   affected patients.

  n   dysautonomic abnormalities, including sweating, hypertension, Sphincter    disturbances are noted in up to one third of patients .

  n   Position sense is the sensory function most frequently impaired, followed  by   vibration, pain, and touch, in descending order of frequency.

   CSF:

  n  An elevation in the CSF protein content is characteristic.

         The CSF cell count is usually normal,

    EMG-NCV:

  n  Demyelinating

  n  conduction block.

  n  prolongation of distal latencies or F-wave latencies,

  n  Decreased conduction velocity.

  n  Axonal

  n  decreased motor action potential amplitude,

  n  preservationof motor nerve conduction velocities,

  n  denervationon EMG,

  n  and normal sensory nerve conduction velocities

 Disorder of neuromuscular transmission

  n  Myasthenia gravis.

  n  Botulism.

 Myasthenia gravis

  n  Myasthenia can begin during childhood ( Juvenile myasthenia).

  n  The onset of juvenile myasthenia can be insidious or rapid

  n  Generally, muscles innervated by the cranial nerves are affected first, with   bilateral ptosis the most common presenting sign

  n  Generalized weakness and dysphagia are less common presenting   symptoms.

  n  The child is usually best in the morning and becomes progressively     weaker during the day.

  n  Despite hypotonia, tendon jerks are normal or even exaggerated, but  they  may disappear after repeated elicitation.

  n  The diagnosis of myasthenia gravis is based on :

  n  a history of abnormal fatigability of voluntary muscles

  n  prompt improvement of muscle weakness with anticholinesterase drugs.

    EMG-NCV:

  n  Rapid stimulation of the distal (ulnar) or proximal(spinal, axillary, or facial)    motor nerves produces a characteristic decrement in the amplitude of   successive action.

  Botulism

  n  Bulbar signs predominate.

        These include a poor cry, poor sucking,

  n  an impaired pupillary light response, and external ophthalmoplegia.

  n  As the illness progresses, a flaccid paralysis develops.

  n  Autonomic dysfunction can be present;.

  n  The EMG shows a pattern of brief duration, small-amplitude potentials with   decremental response at low-frequency (3 to 10Hz) repetitive stimulation,and an  incremental (staircase) response at high-frequency

  n  (20 to 50 Hz) repetitive stimulation (

  Tick paralysis

  n  Tick neurotoxin blocks deoolarization

  n  Motor symptoms include weakness, loss of coordination, and sometimes   an ascending paralysis resembling Guillain-Barre syndrome.

  n  Tendon reflexesa re lost.

  n  Sensory symptoms of tingling paresthesia may occur in the face and   extremities. 

  n  Neurophysiologic studies disclose low-amplitude compound muscle  action    potentials with normal motor and sensory conduction velocities .

  Disorder of muscle

  n  Acute viral myositis.

  n  Acute inflammatory myositis.

  n  Metabolic myositis.

  n  Periodic paralyses.

  Metabolic myopathy

 n  Glicogen storage disease(10 type)

 n  Purine metabolism disease

 n  Lipid storage disease

 n  Mitochondrial disease.

 Idiopathic inflammatory myopathy

  n  Dermatomyositis

  n  Polymyositis: >20yr.

  n  Inclusion body myositis:>50yr.

Diagnosis

Acute viral myositis