Laughing Death, kuru disease

By Hunaina Ali

LAUGHING DEATH is also known as KURU, it is extremely rare, fatal disease, usually resulting from cardiac arrest or asphyxiation, caused by a fit of laughter. It was first discovered in 20th century. It is first mentioned by Australian doctor Zigason and American scientist Carleton Gajdusek. Basically, this disease originated from the fore tribe of New Guinea. The members of this tribe initially believed that this disease appeared as a result of an evil eye created by an alien shaman. However, the truth is actually extremely gruesome and also the people of this tribe perform canabalistic rituals during their funerals because they believed that they could inherit the intellect and other qualities of a person who died if they ate their corpse. Women and children usually perform this ritual so, the disorder commonly found in them.


It is neurodegenerative and transmissible prion disease, cause physiological and neurological effects which ultimately leads to death. The main cause of this disease is abnormally folded prion protein.


People with this disease show symptoms such as tremors, loss of coordination and muscles twitching and impulsive movements of the head that are often accompanied by laughter, they also have eating and walking difficulties. The question arises, why is kuru called the laughing disease? Due to the body tremors that are a classic symptom of the disease and kuru itself means “trembling”. It is also known as the “laughing sickness”. Other symptom include pathological burst of laughter which is the reason we called it laughing death.

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This disease develop in a person through three stages, at the start, they can feel a headache and joint pain they can also experiences loss of control over the body. The second stage is marked by inability to walk and tremors starts to happen more often. Once the disease develops further and moves on to the third stage, the person lose ability to speak and stops eating due to difficulty in swallowing.

Alice (Female) patient aged 56 years when examined in the village, her symptoms began with leg pain, joint pain in her knees and difficulty walking. Her speech and vision had been normal. There was no past medical history of note and she was taking no medications. Her father had been killed by ‘friendly fire’ during clan fighting, which led to her mother, then pregnant with her, fleeing to a neighboring linguistic group, where she was born and grew up. She visited her paternal village in the South Fore with her mother during childhood and moved back there at her marriage. Her mother died in the adoptive community but the cause was not known to her or her relatives. Her husband were also died because of an unknown cause. She had seven children, all of whom are alive and well, and four grandchildren.

On examination, she was responded well to questioning. There was no emotional lability or gross cognitive impairment. There was no dysphasia. The limbs were hypertonic with jerky rigidity, pipe-like in quality, noted equally in both arms. There was no dysmetria in the upper limbs, intention tremor or dysdiadochokinesis. Heel–shin testing was performed well until the feet came together in the midline. No sensory abnormality was detected and proprioception was normal.

Her gait was wide based but she was able to walk independently if supported by a stick. There was marked astasia with clawing of her toes. A clinical diagnosis of stage 1B kuru was made (stage 1 can be subdivided into 1A where the patient can walk entirely unaided, and 1B if a stick is necessary to walk). At the very end of the first stage of kuru, she showed clear evidence of fully established midline cerebellar disease and some extrapyramidal features. Unusually, there were no signs at that time of neocerebellar involvement. The first stage of kuru lasted 17 months. During the next month, he followed a progressive course with worsening cerebellar ataxia typical of kuru, and by the end of 18 month, she had entered the second (sedentary) stage. After three months, she was unable to sit without support and became recumbent (stage 3 of kuru). He alternated between periods of confusion and lucidity. Her disease progressed quite rapidly over the next five months until she died.

Historical Instances of Kuru:

Instances of death by laughter have been recorded from the times of ancient Greece to the modern day. Approximately 2,700 people died due to this disease.
This is a list of notable people who have died from laughter.

Zeuxis, a 5th century BC Greek painter died from laughter.

In 1410, King Martin of Aragon died from uncontrollable laughter.

In 1556, Pietro Aretino died of suffocation from laughing too much.
In 1660, Thomas Urquhart died laughing upon hearing that Charles II had taken the seat.
Pauper, Mr. Arthur Cobcroft and Alex Mitchell are died from a fits of exclusive laughers, which lasted 5-10 min then they would die.


It is concluded that laughing death (kuru) is a degenerative disease of nervous system, restricted to certain tribes in New Guinea, marked by loss of muscular control and thought to be caused by slow virus and transmitted by ritually eating the brains of dead kin.