Disorders of the PNS II (GBS & Bells Palsy) Flashcards
What is the diagnosis of the following clinical manifestation?
- Symetric distal flaccid paralysis evolved in 3 days
- Decreased DTR
- unstable BP
- OH
- Paresthesia
- impaired vibration and position.
- increased pain at night on gluts and hamstrings
GBS
percentage of GBS patients that die due to secondary complications (resp., card, or other systemic organ failure)?
5%
Is it Bell’s Palsy if the pt is able to close eye an wrinkle forehead?
No, UMN lesion (central lesion)
how long is the progressive phase of subacute inflammatory demyelinating polyradiculoneuropathy (GBS)
4 - 8 weeks progressive phase
GBS diagnosis:
- Clinical Signs & Symptoms
- Lab results:
- Normal WBC
- Elevated protein
- h/o flu-like preceding onset of symptoms
- CSF of normal WBC count and increased protein level
- Abnormal NCV
What is Acute Inflammatory Demyelatimg Polyradiculoneuropathology?
GBS subtype, most common
The LMN (Bells Palsy) involvement of the facial nerve can be differentiated from an UMN involvement of this nerve because with UMN involvement the patient can…
- close the eye and wrinkle the forehead but cannot smile voluntarily.
- With LMN involvement, the client Is unable to close the eye, wrinkle the forehead, or smile voluntarily.
Acute forms of GBS:
- Acute motor axonal neuropathy: axon affected
- Acute autonomic neuropathy
- Acute motor & sensory axonal neuropathy
- Miller Fisher syndrome
2/3 cases of GBS have autonomic impaiments including:
- impaired CO
- arrythmias, OH
- unstable BP
- peripheral pooling
- impaired venous return
- ileus
- urinary retention
What is the current Tx of choice for GBS:
Intravenous immunoglobin (IVIg)
80% GBS patients become ambulatory within how long?
6 months of onset
GBS affects what?
nerve roots and peripheral nerves
Rehabilitation Considerations of Bells’ Palsy:
- Electrical Stimulation to facial muscles
- Cold laser
- Neuromuscular reeducation using sEMG biofeedback
how long is the progressive phase of chronic inflammatory demyelinating polyradiculoneuropathy (GBS)?
more than 8 weeks
Which GBS Tx is Indicated for pt with severe respiratory involvement?
Plasmapheresis (Plasma Exchange)
Medical interventions for Bell’s Palsy
- Corticosteroids: prednisone
- Antiviral medications
- Nerve root decompression surgery (rare)
- Eye care (artificial tears)
What is the incidence of Bell’s Palsy and GBS?
- Bell’s Palsy is 20/100,000
- GBS is 2/100,000
Diagnosis of Bell’s Palsy based on what?
- Clinical presentation
- electrodiagnosis test: diff bet axonal or demyelation
- test facial nerve excitability
- diff between UMN and LMN involvement
how long is the progressive phase of acute inflammatory demyelinating polyradiculoneuropathy
4 weeks or less
- multifocal motor neuropathy with conduction block
- chronic relapsing axonal neuropathy
- Are characteristics of what type of GBS?
chronic inflammatory demyelinating polyradiculoneuropathy
Acute unilateral weakness of facial muscles due to inflammation within the fallopian canal OR inflammation of CN VII (facial n):
Bell’s Palsy
What is the underlying cause of Bell’s Palsy?
- Ischemic condition of nerve
- Viral or Bacterial
- Autoimmune disorder
- Anoxia to nerve results in marked edema: vasodilation, transudation of fluid, further pressure effects
Brighton Diagnostic Criteria for GBS:
- Bilaterla flaccid weakness of limbs
- Decreased or absent DTR in weak limbs
- Monophasic course onset-nadir 12h to 28 days
- CSF count <50/microl
- CSF protein > normal
- NCS
- Absence of alternative diagnosis
Tretament of GBS:
Immunotherpay bases Tx:
-
Plamapheresis:
- Mild: 2 sessions.
- Severe: at least 4 sessions
-
Intravenous immunoglobin
- 2g per Kg of body weight over a 5 day period.
What are the most common long term deficits of GBS?
- Weakness of ant. tibialis
- Fatigue/poor endurance
- Some pt, sensory deficits 3-6 years after recovery
Course/Prognosis of GBS:
- Weakness develops 12h to 28 days. Should not porgress after 4 weeks
- 50% of pt experience worse S & S within one week of onset
- Recovery begins 2 - 4 weeks after plateau
- Recovery occurs prox. to distal
- 80% of pt amb within 6 months of onset
- 65% -75% return to normal function
- Some with sensory deficits 3- 6 years after recovery
How many GBS patients return to clinically normal function?
65% to 75%
Recent research identified ___________ as most frequent cause (60% - 70% of cases) of Bell’s Palsy
Herpes simplex virus (HSV-1)
Sensory impairments of GBS include:
- mild
- distal hyperesthesia,
- paresthesia
- numbness
- impaired vibration & position,
- often stocking and glove pattern
Rehabilitation Considerations of GBS:
- Facilitate resp, speech, and swallowing funct.
- Reduce pain (modalities)
- Prevent secondary complications (PROM)
- Maximize function
- Reasses muscle weakness
- Awareness of fatigue levels
- Psychological concern
Risk factors of Bell’s Palsy:
- Diabetes mellitus
- Pregnancy
- Conditions that compromise the immune system
- Previous history of Bell’s Palsy
- 5 – 10% recurrence
- Average 10 yr time span between recurrences
Clinical manifestation of Bells’s Palsy:
- eye does not close
- unilateral peripheral facial weakness
- asymetrical face appearance
- sometimes accompanied by aching pain by jaw or behind ear
- loss of taste on the affected side
- autonomic fiber affected (dry eye, decreased saliva production)
- sounds seem lauder
- crocodile tear syndrome (motor synkinesis)
Prognosis of Bell’s Palsy:
- good recovery
- recovery begins at 1 week of onset
- 75% fully recovery over several week to 3 months
- If recovery takes more than 3 months, usually see more severe residual deficits
- Poorer outcome if:
- >60 y/o
- Hypertension
- Autonomic involvement
- If no recovery: plastic surgery to restore facial function
how long is the progressive symptoms of acute GBS? (how long does it take to get at its worse?
4 weeks or less
Normal CSF white blood cell and increased protein levels (albumin) count help differentiate what disease?
GBS
GBS Clinical Manifestations:
- Symmetric, progressive, distal to proximal wekaness or flaccid paralysis. Often rapidly evolving 12h to 28 days
- Areflexia
-
Possible CN and respiratory involvement:
- 50% CN involvement
- 25% need artificial ventilation
- Autonomic impairments: impaired CO, arrythmias, OH, unstable BP, peripheral pooling, impaired venous return, ileus, urinary retention
- Sensory Impairments: mild, distal hyperesthesia, paresthesia, numbness, impaired vibration & position, often stocking and glove pattern
- Pain: muscle aching type, increased at night, symmetrical, on large bulk muscles
