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Focal lingual dystonia, urinary incontinence, and sensory deficits secondary to low voltage electrocution: case report and literature review
  1. J R Baskerville,
  2. S A McAninch
  1. Scott & White Memorial Hospital and Clinic, Scott, Sherwood and Brindley Foundation, Temple, Texas, USA and The Texas A&M University Health Science Center College of Medicine, College Station, Texas, USA
  1. Correspondence to:
 Dr J R Baskerville, Scott and White Memorial Hospital, 2401 South 31st Street, Temple, Texas 76508, USA


Electrocution injuries are well reported in review articles and cases of high voltage electrocution injury are abundant. However, reports of low voltage electrocution injury are few. A case is presented of low voltage shock from a 120 volt AC source with presentation, acute and chronic course, and a five year follow up. The patient experienced several unusual complications of low voltage electrocution: a persistent right tongue deviation, which initially presents as an isolated hypoglossal nerve palsy, but subsequently manifests as a focal lingual dystonia; total body paresthesia with urinary incontinence; and persistent sensory deficits to the face and tongue.

  • focal lingual dystonia
  • electrocution
  • nerve palsy
  • tongue deviation
  • temporomandibular joint

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Electric shock is a relatively uncommon form of trauma, but is responsible for 7% of traumatic occupational deaths in the United States.1 The severity of electric shock injury is dependent upon many variables: type of current (alternating current or direct current), level of applied voltage, duration of shock, body contact surface area, resistance of tissue involved, contact with water or metal conductor, and current pathway through the body.2,3 Medical literature typically categorises electrocution according to the level of applied voltage: low voltage (less than 1000 volts) and high voltage (greater than 1000 volts). High voltage shock is responsible for the majority of persistent4 and severe5 complications of electrocution. Lightning strikes are a special category of high voltage shock (greater than 100 million volts) and are discussed elsewhere.4,6,7 Low voltage electric shock accounts for 60% to 70% of reported electrocutions,8 and most resultant complications are relatively minor and transient. We describe a case of low voltage electrocution with some common transient complications, and, more notably, a persistent right tongue deviation; three incidences of total body numbness with urinary incontinence; and chronic sensory deficits to both the tongue and face.


A 21 year old white woman with no significant past medical history was attempting to change an overhead light bulb at work while standing on a plastic chair. She received a low voltage shock for an unknown duration of time while touching a screw on a 120 volt AC light fixture. Her hands were dry. She was wearing sandals and had dental fillings at the time of shock. Witnesses state she “jerked backwards,” possibly fell, and did have loss of consciousness for several minutes without seizure activity. However, she denied any memory of falling or loss of consciousness. She reported a feeling of confusion and a metallic taste in her mouth after the injury. She then walked into an adjacent office, where a coworker noticed her slurred speech, a right deviated tongue (fig 1), and bleeding from both ears. She was transported to our emergency department (ED), where she developed a headache, which soon resolved with no complications. A 0.5 cm second degree burn to the left second digit was present with no obvious exit location. ED examination confirmed a right tongue deviation, with dysarthria. A slight right deviation of the uvula was present, but the soft palate elevated symmetrically with a positive gag reflex. Cranial nerves II-XI were intact. She demonstrated 5/5 bilateral extremity strength, and deep tendon reflexes were 2+ and symmetric. No significant sensory deficits were noted, but she reported “numbness to right inside of mouth.” Trigeminal sensation was intact bilaterally to fine touch, vibration, and pinprick. No cerebellar deficits were noted. Tympanic membranes were intact bilaterally with no hemotympanum. Minor lesions to bilateral external auditory canals were present, which the patient stated were caused by aggressive q-tip use after the shock. Computed tomography of the head was negative for haemorrhaging or ischaemia. Magnetic resonance imaging (MRI) was negative for basilar skull fractures or other anomaly. Electrocardiogram showed normal sinus rhythm with no ectopy. Laboratory investigations were as follows: glucose 87, Na 143, K 3.6, Cl 111, C02 26, blood urea 2.5 mmol/l, creatine 0.9. The creatine kinase (total) was increased at 348 (normal 0–225). She was admitted for overnight observation with an impression of cranial nerve XII palsy secondary to electrocution. She was released from the hospital with little change in symptomology, and referred to the neurology clinic.

Figure 1

Right deviated tongue after low voltage electrical shock.

A neurology consultation four days after injury revealed that the right tongue deviation was still present, although not as prominent, and again assessed to be attributable to electrically induced hypoglossal nerve damage. However, neurological examination noted that the initial MRI revealed her cranial nerve XII to be “visualised and intact.” The uvula deviation and facial numbness were absent on this encounter. Also, the patient's mother commented on her daughter's recent memory deficits, such as forgetting previously memorised phone numbers. The patient denied any cognitive or memory impairments. The neurologist was unable to demonstrate significant cognitive deficits, including memory deficits.

The patient complained of dysarthria and dysphasia, which was secondary to decreased tongue mobility.

On neurological examination five weeks after injury, her tongue continued to deviate to the right as before, but she now described a “twitching” of her tongue. The twitching was not a fasiculation-like movement, but rather a “tonic and phasic dystonic movement,” which pulled the tongue to the right. She was rediagnosed with an isolated lingual dystonia, and then was prescribed carbamazepine. Also, she reported right temporomandibular joint (TMJ) pain and difficulty controlling jaw movements. An oral surgery consultation concluded that her TMJ pain was attributable to fatigue of the right masseter muscle, which she consciously manoeuvered to compensate for the right tongue deviation. Significantly, our patient reports three incidences of feeling “numb all over and blacking out” with urinary incontinence beginning approximately one week after the shock. These incidences ceased concurrently with the initiation of carbamazepine. Interestingly, they did not reoccur after carbamazepine was discontinued.

Twelve weeks after injury, the patient reported little relief of dystonic movements from the carbamazepine; it was discontinued and trihexyphenidyl HCl was prescribed, which was also inefficacious in relieving the dystonic movements. The patient was referred to a movement disorder clinic 21 weeks after injury for evaluation of her lingual dystonia, where 15 units of botulinum toxin (Botox) were injected to the submentalis muscle. A follow up visit with neurology 24 weeks after injury revealed decreased right tongue deviation, and the patient was able to move the tongue midline and to the left side “if she concentrated.” She visited a second movement disorder clinic 32 weeks after injury, noting only moderate tongue dystonia and tongue deviation, with no TMJ pain present. The second 15 unit Botox dose was injected into the mylohyoid region this time, which apparently was ineffective. She was then referred back to the first movement disorder clinic 41 weeks after injury, where she received a third and final Botox injection. In a phone interview five years after the shock, she reported no tongue deviation; however, she still reports an occasional temporary “jerking” of the tongue to the right. She states her tongue and right side of face continue to feel “numb and tingle” daily for about 15 minutes upon awakening. Also, her husband states she has a “drooping right eye lid.” She states she is taking no medication currently, and has no further medical complaints, including muscle weakness and additional sensory deficits.


Witnesses did report loss of consciousness without seizure-like activity for a matter of minutes after the injury. It is unclear whether the loss of consciousness was attributable to the electrocution or secondary to a fall from the chair. Transient loss of consciousness is the most commonly reported complication of electrocution—independent of voltage level.2,5 Our patient reported a transient headache, which is another common complaint immediately after electrocution.5

Interestingly, three very unusual sequelae of low voltage shock are reported here. Firstly, the patient reported some “numbness” to the right side of her face. However, ED examination after injury revealed trigeminal sensation objectively intact. The patient states this numbness continues to this day, and occurs daily upon awakening for approximately 15 minutes. It is significant that most low voltage injuries are temporary. Although temporary decreases in sensation are also reported after shock,5 the persistence of this condition secondary to electric shock is quite unusual. Secondly, she reported three separate incidences of total body “numbness” followed by syncope and urinary incontinence approximately one week after injury. These incidences resolved after taking carbamazepine, and did not resume after carbamazepine was discontinued. Although bladder disturbance is reported in a 34 000 volt shock,9 I am unable to locate any reports of urinary incontinence, or total body “numbness associated with low voltage shock.” Thirdly, of notable importance is the isolated right tongue deviation. This non-painful tongue deviation began approximately three minutes after the injury and persisted for nearly one year. Again, it is significant that most complications of low voltage injury resolve quickly. This tongue deviation was initially assessed as an isolated 12th nerve palsy. No reports of electrocution induced 12th nerve palsy are present in reviewed literature. Initially, this tongue deviation was not accompanied by the signs typically associated with cranial nerve XII palsy, such as tongue atrophy, weakness, and fasiculations.10 However, five weeks after injury, tonic and phasic dystonic tongue movements, which “pulled” the tongue to the right, were noted and instead suggested a dystonia of the lingual musculature. Dystonia is an infrequent consequence of electric shock. However, there are rare reports of torticollis and limb dystonia secondary to low voltage electrocution.11 This is the first known instance of focal lingual dystonia secondary to electrocution reported.12 Botulinum toxin is known to be a beneficial agent in treating lingual dystonia.13,14 Subsequent to rediagnosis, the patient was treated with three botox injections, which “resolved” the lingual dystonia. Months after botox treatments, the tongue rested at the midline and she could willfully move her tongue to the left. Her dysphasia, dysarthria and TMJ pain ceased with the resolution of the tongue deviation. However, she still complains of occurrences of her tongue “jerking to the right” for about 15 minutes each morning, which resolves on its own.

Other transient complications of low voltage shock are published: homonymous hemianopia 15; seizures,5 specifically grand mal 16,17; muteness 18; transient qaudraplegia 18; left hemiplegia 15; left hemiparesis and general motor weakness 15; reflex sympathetic dystrophy 19; ventricular fibrillation 20; abdominal visceral injuries 16,21; scapular fracture 16; and carpal tunnel syndrome.19 Rare occurrences of delayed onset and chronic sequelae secondary to low voltage electrocution, such as amyotrophic lateral sclerosis/motor neurone syndrome and impotence, are documented.22,23 Fatalities are reported at voltage levels as low as 46 volts and 60 volts,18 and low voltage sources are often the chief mechanism of accidental death in the home.8


Serious complications of electric shock typically result from high voltage shocks such as power lines and lightning strikes. Although most low voltage electrocutions result in minor and ephemeral complications, this case presents three highly unusual sequelae: incidences of total paresthesia, followed by syncope and urinary incontinence; chronic sensory deficits to the face and tongue; and a persistent focal lingual dystonia. This case provides further evidence that low voltage sources can cause unusually debilitating and unremitting complications, and should be considered a greater potential danger than conventionally thought by clinicians. Considering that low voltage electrocutions primarily occur in the household, and account for 1% of accidental deaths in the home,8 this case also proves the need for greater emphasis on electrical safety in the home to prevent such potentially dangerous injuries.


I would like to express my appreciation to Richard Lenehan, MD for his assistance and guidance.

 Jerry R Baskerville, MD, (guarantor and first author) was the treating physician. Dr Baskerville archived the patient data initiated and coordinated the writing of this manuscript. Scott A McAninch (second author) provided patient follow up, performed the literature research, and compilation of the manuscript.