Nocturnal Paralysis and Tingling

Randolph W. Evans, MD, Howard W. Sander, MD


February 20, 2003


Parasomnias are a fascinating group of clinical disorders associated with undesirable physical and mental phenomena that occur predominantly during sleep. They include sleepwalking (somnambulism), night terrors, confusional arousals, sleep paralysis, sleep starts or hypnic jerks, sleeptalking (somniloquy), bruxism, nocturnal leg cramps, and sleep enuresis.

Parasomnias are common. Sleep starts, myoclonic jerks occurring in the transition from wakefulness to sleep, nightmares, and bruxism are almost universal during a person's lifetime. Sleepwalking occurs in about 30% of children aged 4-6 years old and 2% of adults. Night terrors (also called "pavor nocturnes" in children and "incubus" in adults), which usually manifest as screaming and agitated behavior with attempts to leave the bed or the room lasting 1-5 minutes, occur in up to 6% of prepubertal children and 2% of adults. Sleeptalking occurs frequently in about 10% of children and less often in adults. Nocturnal leg cramps are particularly common among teens and the elderly and during pregnancy. The following case raises interesting issues in diagnosing parasomnias.


A 33-year-old woman 3 months pregnant presented for evaluation of sleep-related complaints. Earlier that day, she woke up partly awake from sleep in the middle of the night with tingling from the head to the toes, particularly intense in the head. She could not move or talk for about 30 seconds. She then was fully awake and all the symptoms were gone but she felt nervous. About 20 minutes later, as she was falling back to sleep, she had tingling of both lower extremities for about 20 seconds but was able to move. She then fell asleep. She felt fine the next day. There was no history of similar sensory symptoms, sleep paralysis, or myoclonus. Past medical history was negative. Neurologic examination was normal.

Question: What is the diagnosis? Is diagnostic testing indicated?


This patient presented with 2 brief nocturnal episodes occurring 20 minutes apart in the middle of one night. The first episode occurred upon awakening and included paralysis and dysesthesias, and the second episode occurred upon falling asleep 20 minutes later and involved purely dysesthesias.

As these symptoms were brief and occurred once, it is difficult to arrive at a conclusive diagnosis. The differential diagnosis includes sleep paralysis, transient ischemic attacks, seizures, sleep starts, or other parasomnias. The first episode had the motor features of sleep paralysis, but was associated with positive sensory phenomenon. Sleep paralysis (partial or total paralysis that may be accompanied by inability to speak) may occur either upon sleep onset or awakening, and may occur in isolation in 30% to 50% of normal subjects.[1] However, sleep paralysis is not traditionally associated with concomitant sensory symptoms,[2] precluding a definite diagnosis of sleep paralysis for the first episode. The second episode occurred upon sleep onset and consisted purely of sensory phenomenon. This episode is reminiscent of sensory sleep starts. This benign condition has been reported to occur only at sleep onset and consists of recurrent episodes that may involve a variety of sensory features including: brief light flashes, fragmentary visual hallucinations, visual hypnagogic dreams, loud noises, pain, paresthesias, dysesthesias, numbness, a floating sensation, or a perception of something "flowing through the body."[3] Sensory sleep starts may occur in isolation,[3] or they may be associated with the more commonly described predormital myoclonic jerks that are often simply referred to as sleep starts.[1] In the current patient, the second episode may, in fact, have been a sensory sleep start; however, this diagnosis cannot be conclusively established as it occurred only once. Additionally, the occurrence of an immediately preceding episode of paralysis with a similar dysesthetic sensation suggests that the second episode may have been a variant of the first episode, rather than a separate entity.

Differential diagnostic possibilities of seizures or transient ischemic attacks may also be considered, but cannot be definitively established, as the episodes were quite brief, did not implicate a specific cerebral vascular distribution, and were not accompanied by clonic movements.

As the symptoms did not appear to suggest future serious sequela, observation would be reasonable. An electroencephalogram could have been considered, although this would likely have had a very low diagnostic yield. Assuming no additional episodes occurred by delivery, no further intervention would be needed. In that case, the most likely diagnostic possibilities would have included: atypical form of sleep paralysis, sensory sleep start, or another atypical parasomnia. If further episodes occurred, and the symptoms were sufficiently bothersome, the next management step would be a sleep specialist consultation with consideration of a polysomnogram.

In clinical neurology, single-episode, brief phenomenon are often described by patients. In these cases, a clear diagnosis frequently is elusive, as the distribution of dysfunction may not suggest a clear anatomic localization, the episode may be incompletely described, and there are no physical examination or laboratory study abnormalities to suggest a specific cause. Clinicians often wisely opt to manage conservatively and observe for further events, rather than pursue low-yield diagnostic testing that could entail the risk of false positive results.

Follow-up: The patient was reassured about the benign nature of her symptoms. Diagnostic testing was not performed. On telephone follow-up 2 years later, she had had no further episodes.


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