Facial palsy

A generalized systemic illness may accompany HIV seroconversion (Cooper et al. 1985). Guillain-Barre syndrome (GBS) (Piette et al. 1986), unilateral (Wiselka et al. 1987) or bilateral facial palsies (Wechsler and Ho 1989), bibra-chial palsy (Calabrese et al. 1987) and sensory neuropathy (Denning 1988) have been reported to occur during this process, usually within 1-2 weeks of the acute febrile illness. Spinal fluid analysis may show a mild to moderate mononuclear pleocytosis and a mild increase in protein levels. The precise relationship to HIV viral load in the cerebrospinal fluid (CSF) or plasma is unknown (Brew 2003). There is no proven therapy, but most patients recover spontaneously without any treatment. 

Facial palsy 0 = normal 1 = minor 2 = partial 3 = compete... 

Neurologic symptoms (meningoencephalitis, aseptic meningitis, peripheral neuropathy, facial palsy, or cognitive impairment or psychosis)... 

Peripheral neuropathy primary dose-limiting toxicity motor sensory, autonomic, and cranial nerves may all be affected (paresthesias, ileus, urinary retention, facial palsies) may be irreversible mild emetogen SIADH vesicant extravasation injury... 

Nagano T, Mizngnchi M, Kurihara E, Miznno Y, Tamagawa K, Komiya K. [A case of acnte disseminated encephalomyehtis with convulsion, gait disturbance, facial palsy and multifocal CT lesions.] No To Hattatsu 1988 20(4) 325-9. 

An unexplained case of permanent neurological deficit, consisting of left facial palsy, right sensorineural hearing loss, gait ataxia, and hemisensory loss in the body and face, has been described after inferior alveolar nerve block (93). 

In general, the incubation period in humans after tick exposure is 7-14 days. The characteristic symptom seen in most infected individuals is a red, slowly expanding, bulls-eye rash. This is accompanied by general malaise, fever, headache, muscle aches, and joint pain. If the infection is not treated, the exposed individual may develop arthritis, neurological symptoms e.g., facial palsy, nerve, and/or brain inflammation and, rarely, cardiac abnormalities. 

The toxin(s) can cross the placenta, and children born of mothers who have been affected late in pregnancy may manifest bizarre fetal movements in utero and facial palsies after delivery. Maternal hyperesthesia of the nipples may interfere with breast feeding (Pearn et al. 1982). 

The presentation of RVD in childhood is variable. Occasionally a child is incidentally found to have high blood pressure (BP) on routine examination. The diagnosis is often delayed due to technical problems in measuring the BP and a low index of suspicion in children (Tullus et al. 2007). BP measurements should always be compared with published standards for age, sex and height (Goonasekera et al. 2000 Rosner et al. 1993). Other presentations may relate to secondary effects of hypertension, such as cardiac failure, an isolated lower motor neuron facial palsy, severe headaches or failure to thrive. 

DIES-associated neuropathy has a variety of chnical presentations, including painful symmetric or asymmetric sensorimotor neuropathy, distal sensory neuropathy, mononeuritis multiplex, and demyelinating polyneuropathy (Gherardi et al. 1998). Cranial neuropathy without evidence of a more generahzed neuropathy may occur, typically as a facial nerve palsy in association with parotidomegaly (Itescu et al. 1990 Brew 2003). The neuropathy develops subacutely over days to weeks. In some cases, muscle weakness may be a result of an inflammatory myositis (Kazi et al. 1996). 

Cameron C, Lodes MW and Gershan WM. 2007. Facial nerve palsy associated with serum vitamin A level in an infant with cystic fibrosis. J Cyst Fibros 6 241-243. 

Peak blood levels occur within 15 minutes after smoking. The effects last for approximately 4 hours, although it may take more than 24 hours for an individual to return to a normal state. The drugs are stored in fatty tissue and released slowly. PCP has a long half-life ranging from many hours to days, and the PCP glucuronide metabolite can be found in urine for several days or weeks. PCP is found in breast milk. The half-life of ketamine is three to four hours, and metabolites of ketamine are excreted in urine. PCP and ketamine cross the placental barrier, and infants of chronic abusers have been born with cerebral palsy, facial deformities, and behavioral abnormalities. 

Bell s palsy It increases the recovery time for facial nerve function in Bell s palsy. 

The therapeutic use of botulinum toxin for ophthalmic purposes and for local muscle spasm was mentioned in Chapter 6. Local facial injections of botulinum toxin are widely used for the short-term treatment (1-3 months per treatment) of wrinkles associated with aging around the eyes and mouth. Local injection of botulinum toxin has also become a useful treatment for generalized spastic disorders (eg, cerebral palsy). Most clinical studies to date have involved administration in one or two limbs, and the benefits appear to persist for weeks to several months after a single treatment. Most studies have used type A botulinum toxin, but type is also available. 

Botulinum toxin A complexed with haemagglutinin is currently employed medicinally to counter involuntary facial muscle spasms, e.g. around the eye. Very small (nanogram) amounts are injected locally and result in the destruction of the acetylcholine release mechanism at the neuromuscular junction. Since new nerve junctions will gradually be formed over two months or so, the result is not permanent, and the treatment will need to be repeated. It has also been found useful in easing muscle spasticity in children with cerebral palsy. 

Two patients, one of whom also received ribavirin, had facial nerve palsy after 5 and 8 months of interferon alfa therapy (59). The palsy resolved completely in one patient after withdrawal and the administration of prednisolone however, in the other case, the palsy resolved without drug withdrawal, suggesting coincidence. 

A 67-year-old man developed transient hemiparesis and facial nerve palsy before becoming unconscious and apneic 10 minutes after a right cervical plexus block (89). His trachea was intubated without the need for anesthetic drugs and he was ventilated. Hypotension was treated with intravenous ephedrine. He woke up, started breathing, and was extubated 75 minutes later. The authors postulated brainstem anesthesia following accidental injection of local anesthetic into a dural cuff as a cause of loss of consciousness. 

More than 140 cases of toxic polyneuropathy have been reported. The frequency depends on dose, tissue concentration, and renal function in up to 90% of cases polyneuropathy occurred in patients with renal insufficiency (32). Symptoms usually start 9-45 days (at the earliest 3 days) after beginning nitrofurantoin. The neuropathy starts peripherally, predominantly affects the limbs, and remains more severe distaUy. Initially, there is sensory loss with paresthesia. Later, motor loss develops, often with severe muscle atrophy. As a rule, no further deterioration occurs after withdrawal of nitrofurantoin, and there may be total regression (34% of cases) or partial regression (45% of cases) (32). In some severe cases there is residual disability. The motor loss resolves more slowly and less completely than the sensory impairment. Single cases of retrobulbar optic neuritis, lateral rectus muscle palsy, and facial nerve palsy have been reported (33). 

A corneal ulcer associated with deposits of norfloxacin in the right eye has been reported in a 40-year-old man with right trigeminal and facial nerve palsies and reduced tear secretion. He stopped using norfloxacin ophthalmic solution and recovered (3). 

Cranial nerves Note facial tone and symmetry, gaze preference, and ptosis check for nystagmus by having patient follow object across visual field engage in conversation to assess for slurred speech. Myasthenia gravis (ptosis), Parkinson s disease (masked facies), stroke (palsy), antiepileptic drug therapy (nystagmus, slurred speech)... 

May result in blindness, deafness, and facial nerve palsies... 

Ear Hemotympanum Vesicles Basilar skull fracture Facial weakness due to zoster-associated Vllth nerve palsy... 

Allergic reactions in the eyelids have been reported in two women who had gold weights inserted to create mechanical ptosis to protect the comeae following facial nerve palsies [60" ]. Gold particles were identified in the tissues and so these were between-the-eyes adverse reactions of type lb [61 ]. 

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