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The International Journal of Stroke
 Hand up! Yawn and raise your arm
Olivier Walusinski
Jean-Philippe Neau
CHU Poitiers (France)
Julien Bogousslavsky
Valmont-Genolier, Glion sur-Montreux, Switzerland


"Arise and walk, or yawn and raise your arm"
Summary : why a paralysed arm raises during yawning?
In some cases of hemiplegia the onset of yawning is associated with an involuntary raising of the paralyzed arm. Six observations of this movement, which is seldom described probably because it is mostly neglected, were made in two neurology units. The descriptions were compared with other cases that have been published in the medical literature of the last 150 years.
Cerebral imagery shows a lesion that is most often localized on the internal capsule. After comparison with experimental models in cats, it is proposed that the section of the corticoneocerebellum tract of the extrapyramidal system disinhibits the spinoarcheocerebellum tract, enabling a motor stimulation of the arm by the lateral reticular nucleus, which harmonizes both central respiratory and locomotor rhythms.
When certain subcortical structures, phylogenetically more primitive, are thus disinhibited, they regain autonomy in the homeostasis process associating the massive inspiration of yawning &endash; a form of reflex behavior that stimulates vigilance &endash; with a motor control that is active during locomotion. For this phenomenon we coined the term "parakinesia brachialis oscitans".
Tous les articles sur la parakinésie brachiale oscitante 
All articles about parakinsia brachialis oscitans
Respiratory and locomotor patterns

In 1844, the following case was reported in "The nervous system of the human body as explained in a series of papers read before the Royal Society of London" by the Scottish physician John Abercrombie (1780-1844), an author well known for his exact observations and reports of their pathology : "I had some time ago under my care, a man affected with hemiplegia of the left side, the palsy complete, without the least attempt at motion, except under the following circumstances: he was very much affected with yawning, and every time he yawned the paralytic arm raised up, with a firm steady motion, until it was at right angles with his body (as he lay in bed on his back), the forearm a little bent inwards, so that his hand was above his forhead at its greatest elevation. The arm was raised steadily during inspiration, and when the expiration began seemed to drop down by its own weight with considerable force. He continued liable to the affection for a considerable time, and it ceased gradually as he began to recover the natural motion of the limb." (Bell, 1844)
Using recent case reports collected from two differents sites in France and Switzerland, we aim to present this curious phenomenon, which involves the combination of involuntary motion in a paralyzed upper limb with yawning. We propose afterward a pathophysiological hypothesis.
Case reports.
Case 1 (Montreux)
A 49-year-old lady with no history of vascular disease or recognized risk factors, except a long history of migraine with aura and cigarette smoking, developed a fluctuating hemiplegia on the left side, shortly after waking up. Weakness predominated in the upper limb, with moderate dysarthria. Sensory testing was unremarkable, and no associated neurologic dysfunction was found on examination. Diffusion-weighted MR showed a small infarct in the posterior limb of the right internal capsule, with associated marked leukoaraiosis. Blood pressure was normal, as were cardiac investigations and extra/intracranial MR angiography. A positive mutation for CADASIL was found (her father had had strokes and dementia). After 2 days, the patient reported that while she was unable to move the left upper limb on purpose, it raised every time that she yawned, up to the level of her breast, when she was in a sitting position. This lasted for a few seconds and was not associated with specific movements of the hand and fingers. The phenomenon could be demonstrated in front of external observers, and disappeared while motor recovery developed over the following two weeks.
Case 2 (Montreux)
A 73-year-old gentleman, treated for high blood pressure and cholesterol, developed sensorimotor hemiparesis on the right side, without cognitive changes or aphasia. Initially, he was completely paralyzed in the upper limb, but during episodes of yawning, the same limb would move upwards for about 30 cm, remain still for a couple of seconds, and then slowly return to its primary position. This was mainly noted when the patient was sitting in a wheelchair, and disappeared after one week, while the patient recovered some voluntary motricity in the upper limb, with ataxia. MRI showed a small infarct in the anterior limb of the left internal capsule, suggesting lacunar infarction. An occlusion of the V4 segment of the left vertebral artery was present, but no large artery disease was found in the anterior circulation, and cardiac tests showed no embolic source.
Case 3 (Poitiers)
A right-handed, 71-year old retired postman and non-smoker was being treated for non-insulin-dependent diabetes and hypercholesterolemia, without hypertension. In November 1996, he presented with an isolated motor deficit in the left leg, resolving in 24 hours. The assessment of this transient ischemic attack revealed bilateral 40%-50% stenosis of the internal carotid arteries, with non-ulcerated atheromatous plaques at the right carotid bifurcation with inhomogeneous echo structure, without thrombi. A few days later, magnetic resonance imaging (MRI) of the brain showed no residual lesions. The echocardiogram was normal. The patient was prescribed 250 mg of aspirin per day. In September 1999, sudden onset of rotatory vertigo was rapidly followed by severe left hemiplegia without sensory impairment and without nystagmus or hemianopsia. The brain CT scan was normal upon the patient's admission. Doppler examination of the neck vessels produced the same results as previously. The Holter ECG recording suggested neither arrhythmia nor ischemia. The transoesophageal echocardiogram revealed a left intra-atrial thrombus. The follow-up CT scan secondarily associated the ischemic-appearing hypodensity in the right semioval center and right lenticular nucleus with leukoaraiosis. The diagnosis was embolic occlusion of the lenticulostriate branches of the right middle cerebral artery. The patient was put on heparin, with a vitamin K antagonist as relay treatment. One year later, the patient still had severe left hemiplegia, predominantly brachiofacial; spasticity was significant. During a follow-up visit, he reported the involuntary lifting of his totally paralyzed left arm during yawning. In 2 to 3 seconds, the arm was raised around 10 centimeters, with adduction and elbow flexion, at the same time as the patient opened his mouth. It fell inert once he closed his mouth. This could occur while he was sitting, standing or lying down. He had observed this phenomenon from the onset of his hemiplegia. In June 2002, three years after the vascular accident, this involuntary movement of the paralyzed arm during yawning persisted.
Case 4 (Poitiers)
A right-handed, 53-year-old male bank employee was known to be a carrier of activated protein C resistance (Factor V Leiden, treated with a vitamin K antagonist). This hemostatic disorder had already caused phlebitis in his right leg in 1999 and 2000. In addition to this thrombosis risk factor, he had a high blood cholesterol level of 2.4 g/L and had smoked around 15 cigarettes a day since age 14. Between May 27 and June 2, 2001, he had a series of alternating transient ischemic attacks, characterized by predominantly brachiofacial motor deficits and requiring hospitalization. The carotid Doppler examination and the echocardiogram were normal; the patient's blood pressure was also consistently normal. On June 6, 2001, heparin was stopped for 4 hours to obtain an angiogram of the supra-aortic arteries. During this period, a severe left hemiplegia with sensory deficit and without hemianopsia developed rapidly and did not resolve. The brain CT scan revealed an infarct in the right caudate nucleus and right semioval center. The angiogram revealed dolichoectasia of the C2 and C3 portion of the right carotid siphon, and a thrombus in the middle cerebral artery at the origin of the lenticulostriate arteries. In the hours following the cerebral infarction, the patient was very drowsy and yawned deeply in an abnormally frequent and repeated way. At the beginning of each yawn, the left arm lifted involuntarily with flexion of the elbow and adduction. This gesture lasted for the duration of the yawn. The muscular force was so great that the patient's wife, seated next to him, was unable to counter it.
Case 5 (Poitiers)
A right-handed, 75-year-old male retired railway worker with alcoholic cirrhosis presented on November 7, 2001, with brachiocephalic severe right hemiparesis resolving in an hour. His blood pressure was 14/8. However, in the days following, his systolic blood pressure was highly variable with several peaks above 20. Because he was living in a geriatric facility, he did not undergo a Doppler examination. The brain CT scan was normal. He received one injection of Enoxaparin 40mg per day. On November 10, 2001, a brachiocephalic right hemiplegia developed, associated with lingual paresis, Broca's aphasia and alliesthesia in the right arm. The patient's blood pressure was 22/10. The Doppler examination found left and right internal carotid lesions which were identical in appearance and consisted of irregular calcified atheromatous plaques. The lesions measured 1.5 cm in height and were non-ulcerated without adherent thrombi, with 50% stenosis, without hemodynamic repercussions. The vertebral arteries were normal. The echocardiogram showed a dilated left atrium, concentric left ventricular hypertrophy, moderate mitral insufficiency and an absence of intra-atrial thrombi. The ECG showed normal sinus rhythm. The CT scan performed on November 19 (D+9) revealed an infarct in the left internal capsule and left lenticular nucleus, without signs of hemorrhage, without mass effect. The ischemia resulted from a thrombus in the middle cerebral artery at the level of the lenticulostriate arteries. From the onset of the patient's accident, an increased frequency of yawning was noted. With each yawn, the right arm lifted with adduction and elbow flexion, falling as soon as the patient closed his mouth.
parakinesie = video
Case 6 (Poitiers)
A right-handed, 35-year-old housewife and smoker presented during the 7th month of her third pregnancy with superficial calf vein phlebitis (June 2003). She received a daily injection of Enoxaparin 40mg for one month. On October 20, 2003, two months after her delivery, under low-dose combined oral contraception, she rapidly developed an inhabitual, diffuse, intense headache resistant to all the peripheral analgesics tried. She did not consult a physician. On October 22, 2003, her husband found her lying on the ground, paralyzed and aphasic. Upon her admission to the emergency room, massive complete right hemiplegia was noted along with total aphasia, bilateral mydriasis with pupils showing little responsiveness, agnosia, an absence of nuchal rigidity, cerebellar syndrome and sensory impairment. The patient was very drowsy and showed a clear automatic-voluntary dissociation. Blood pressure was 12/7 and cardiac rhythm was sinusal. The CT scan performed on admission was normal without subarachnoid hemorrhaging. The Doppler examination was normal on the right. On the left, there was complete occlusion of the internal carotid, with no distal flow. The transoesophageal echocardiogram was normal. A CT scan performed in November 2003 (D+20) and transmitted via teleradiology showed a complete middle cerebral artery territory infarct and contrast uptake in the left frontotemporoparietal cortex. The angiogram showed fibromuscular dysplasia and left carotid dissection, responsible for the complete MCA territory infarct with cortical and subcortical involvement. From the initial phase of complete flaccid hemiplegia, every time the patient yawned, her completely paralyzed right arm lifted with elbow flexion and moved adductively towards her face, before falling heavily when she closed her mouth.
Altough being probably unaware of the publication of J. Abercrombie in 1844, D Liégey of Rambervilliers in France reports in the same manner, in1851, the following case published in the Gazette médicale de Strasbourg: "A man recovering from repetitive attacks of hemiplegia was overcome by very disagreeable yawning which occurred every day at the same time. No less remarkable, whenever this yawning occurred, it was accompanied by a convulsive movement which raised the patient's previously paralyzed arm. The movement produced a painful sensation in the limb and could only be stopped by the patient strongly grasping the arm with the opposite hand."
Hence, since the early 19th century, a few cases of the movement of a paralysed arm during yawning have been reported : E. Darwin 1801, J. Albercrombie & A. Gendrin 1835, Liegey 1851 & 1879, Ogle 1863, R. Trautman 1901, H. Thomson 1903, M. Bertolotti 1905, FM. Walshe 1923, J Purves-Stewart 1931, A. Heusner 1946, G. Mulley 1982, A. Lanari 1983, H. Wimalaratna 1988, O. Blin 1994, E Louwerse 1998, R. Töpper 2003. The etiology is either an ischemic or hemorrhagic vascular accident or a bulbar form of amyotrophic lateral sclerosis; in an earlier case, brainstem tuberculoma was the cause. Based on these cases and the literature review, this hemiplegia-associated movement shows no lateral preference and may appear from the accident's onset during the flaccid phase, or later, during the spastic phase. The reports mention either abduction or adduction of the arm. While the paralysis leaves the arm immobilized in semi-extension alongside the patient's body, we have observed the arm to move outwards away from the thorax (abduction), followed by elbow flexion bringing the hand towards the sternum (adduction). This movement is strictly concomitant with the yawn; the arm falls inert once the yawn ends. No simultaneous movement is observed in the leg. The arm's movement is totally involuntary and uncontrollable. It coincides with the paralysis and tends to disappear if there is motor recovery.
From 1988 on, the case reports have localized the lesion responsible for the paralysis. Two locations appear closely linked to this clinical picture. The first is a lesion in the middle cerebral artery territory, particularly the lenticulostriate branches, leading to infarction in the internal capsule and lenticular nucleus (paleostriatum) or caudate nucleus (neostriatum) (Bladin and Berkovic, 1984). The second is a pontomedullary lesion, as caused by tuberculoma in a 14-year-old girl with Millard-Gübler syndrome (Bertolotti, 1905), and also reported in a series of bulbar amyotrophic lateral sclerosis cases (Louwerse, 1998) and in a case of basilar artery thrombosis resulting in right-sided pontine infarction (Töpper, 2003).
Hemiplegia and associated movements.
At the end of the 19th century, neurologists were already discussing the movements associated with hemiplegia. Vulpian (1866) employed the term synkinesis for "movements which take place involuntarily in one part of the body as voluntary or reflex movements are carried out elsewhere." In pyramidal syndromes in general and hemiplegias in particular, synkinesis produces involuntary movements in paralyzed muscles concomitant with voluntary movements in healthy muscles. Classically, there are several types: global synkinesis, which is merely an exaggeration of the contraction on the paralyzed side during an effort on the healthy side; coordination synkinesis, when the voluntary contraction of the healthy muscle results in the involuntary contraction of the paralyzed synergistic muscles; and imitation synkinesis, when a voluntary movement on the healthy side triggers an involuntary attempt at the same movement on the paralyzed side.
De Buck (1899) also described movements associated with hemiplegia: "Surprisingly enough, they extend even to the extremities of organs not under voluntary control. These processes accompany not only voluntary movements, but also reflex movements &endash; yawning, sneezing, etc." A. Souques wrote about hemiplegia in Pratique Médico-Chirurgicale (Brissaud, Pinard and Reclus, 1907) re-examined this distinction: in addition to synkinesis which only occurs in the spastic phase, "associated reflex movements coincide with a cough, a yawn, primarily affecting the upper limb" and may be observed during the initial flaccid phase. Working in Turin, Bertolotti (1905) made the same distinction. And Brissaud wrote in his lecture dated December 1, 1893: "Spasmodic yawning is also seen with a certain frequency in hemiplegics. Not merely a superficial symptom amongst the spasmodic elements of epilepsy (Féré) or hysteria (Charcot, Gilles de la Tourette, Guinon and Huet), it indeed seems to arise directly from organic lesions...." We agree with the disciples of J.-M. Charcot on this point, and do not support using the term synkinesis to describe this involuntary raising of the arm during yawning.
In vertebrates, ethologists describe pandiculation or Rekel-Syndrom as the association of yawning with a stretching of the trunk and four limbs (Selbach and Selbach, 1953). Bertolotti (1905) and Blin (1994), each reporting similar cases to those described above, use the term pandiculation or hemipandiculation. Neither the description of the arm's involuntary, non-stretching movement, nor the absence of stretching in the leg on the same side, support the use of this term.
De Buck (1899) wrote: "Parakinesia appears to differ from synkinesia by the fact that the relationship between the idea and the act in the latter is perfectly preserved, involving only a simple diffusion of the nervous influx at the motor centers, owing to the need for a much stronger signal to produce a useful effect; in parakinesia, the relationship between the idea and the movement appears disrupted." We have therefore proposed the term parakinesia brachialis oscitans. Parakinesia is an abnormal movement that acts as a parasite, caricature or replacement of a normal movement, in this instance of the arm (brachial). Oscitans comes from the Latin oscitantis, meaning "which yawns" and mentioned in early writings on fever (Thomson, 1827).
Yawning is phylogenetically ancient, resembling to what ethology appoints a maintenance behavior. Highly stereotypical, it is observed in cold-blooded and warm-blooded vertebrates, from reptiles with rudimentary, "archaic" brains to human primates, in water, air and land environments. The ethology, neurophysiology and neuropsychology literature associates yawning with wake/sleep rhythm fluctuations, eating, and sexuality, where it externalizes a group of vigilance-stimulating mechanisms and attests to the hypothalamus' central role in homeostasis (Aubin and Garma, 1988; Daquin et al., 2001; Walusinski and Deputte, 2004). Yawning is recognizable in ultrasound images from the 14th week of pregnancy, and like the appearance of oromandibular movements and swallowing, it signals functional maturation of the brainstem and basal ganglia, whereas the extension of the frontoparietotemporal cortex continues through the 24th week (Abadie et al., 1999). No brain structure has ever been identified as the yawning center. Clinical and pharmacological evidence indicates that the hypothalamus &endash; particularly the paraventricular nucleus &endash; plays a key role in yawning, as well as medullary and pontine regions, with connections towards the frontal region in human primates and towards the cervical spine. The muscles that contract during yawning are supplied by cranial nerves V, VII, IX, X, XI and XII, cervical nerves C1-C4 (phrenic nerve) and the dorsal nerves innervating the intercostals, which play an accessory role in breathing (Chouard and Bigot-Massoni, 1990).
Provine et al. (1987) showed that yawning has no effect on arterial oxygenation. Hence, the old paradigm, which from the time of Hippocrates to the mid-20th century posited this behavior as a reflex to increase brain oxygen supply, must now be replaced with a neuromuscular paradigm involving subcortical control. The hypothalamic paraventricular nucleus contains the cell bodies of oxytocin neurons projecting to the hippocampus and to the reticular formation and locus ceruleus in the brainstem. When these neurons are stimulated by dopamine, excitatory amino acids or oxytocin itself, they trigger yawning by releasing oxytocin in these various subcortical structures. This oxytocinergic activation is inhibited by opioids, which prevent yawning. The activation or inhibition of these oxytocin neurons is correlated with the activity of paraventricular nitric oxide synthase. Other neuronal systems are involved as modulators. Serotonin, estrogens, testosterone and hypocretin play a role either in the paraventricular nucleus or the motor nuclei of the brainstem and spinal cord, with the final executive pathway controlled by acetylcholine (Argiolas and Melis, 1998; Blin, 1996; Sato-Suzuki et al., 2002).
Attempt at a pathophysiological explanation.
The release of subcortical structures from cortical inhibition is classically proposed to explain certain automatic or reflex activities occurring experimentally in decorticate animals or following stroke in humans. This is the case for palatal myoclonus, or palatal tremor (Lapresle, 1984), caused by destruction of the central tegmental tract, allowing uncontrolled activity in the olivary body and, in turn, the palate's rhythmic movement. This amounts to a reemergence of the structure's phylogenetically branchial function.
Another example is the syndrome of Foix, Chavany and Marie (1926), or biopercular syndrome, where the automatic activities of emotional expression, swallowing and yawning remain intact even though there is total faciopharyngoglossomasticatory paralysis. The automatic activity depends on the brainstem and is preserved, whereas the voluntary control of the prerolandic cortex and the supplementary motor area is interrupted by a biopercular infarct. One MRI case study showed this automatic-voluntary dissociation as a corticobulbar disconnection (Ghika and Bogousslavsky, 2003).
A final example is locked-in syndrome, in which there is total paralysis and patients may only retain voluntary control over eye movement. However, involuntary facial expressions of pain are preserved, along with yawning and loud crying. The corticospinal or pyramidal tract is completely interrupted at the pons. The preserved activity of extrapyramidal and cerebellar structures and of archaic spinal automatisms explains the automatic-voluntary dissociation (Bauer et al., 1980).
Could such a mechanism of cortical-subcortical dissociation explain the synchronization between the raising of the arm and the respiratory cycle of the yawn, due to diaphragmatic extension?
The study of the relationship between respiratory cycles and movement was initiated by Marey (1892) through his invention of chronophotography, a precursor to the cinema. He had already shown that the breathing cycle of a running dog, a galloping horse and a flying gull was based on stride or wingbeat. This synchronicity allows optimal adaptation between oxygenation and muscular work, but the resulting piston effect of the diaphragm's movement also plays an important role in bodily and aerodynamic equilibrium. Energy transfers between trunk muscles and those used for breathing improve the energetic yield of running (Bramble and Carrier, 1983; Hsueh-Tze, 1997; Viala, 1986). Humans maintain partial coupling with arm-swinging during walking, a sign of extrapyramidal activity (Persegol et al., 1991; Bernasconi and Kohl, 1993).
Respiratory automatisms are the result of several medullary and pontine nuclei working in concert. Experimental data suggest that respiratory rhythm generation depends on pacemaker neurons. These neurons are found in a small region known as the pre-Bötzinger complex, ventral to the nucleus ambiguus and to the emergence of the roots of cranial nerve XII. The pacemaker-generated rhythm is modulated by networks of respiratory interneurons, responsible for its final spatiotemporal organization. Inspiratory and expiratory neurons have been described according to the respiratory phase concurrent with their firing time. The rhythmic signal from these neuronal interactions is then distributed, according to a precise spatiotemporal pattern, to medullary and spinal motor neurons, thereby ensuring the motor innervation of the upper airway and respiratory muscles (Bianchi et al., 1995; Duffin and Ezure, 1995).
Adjacent to these nuclei, the lateral reticular nucleus projects to the cerebellum and plays a role in the sensory-motor coordination of the limbs. This corresponds to the spinoreticulocerebellar pathway. Experiments in the cat have shown that when the nuclei in the respiratory rhythm complex are firing, the lateral reticular nucleus itself has a rhythmical and synchronous activity, particularly when limb extensor muscles are contracted during stretching (Arshavsky, 1978 and 1986; Ezure and Tanaka, 1997; Richard and Waldrop, 1989). The dual role of the intercostals and the diaphragm in posture and locomotion on the one hand, and in breathing on the other (not to mention phonation), requires not only somatomotor coordination, but also neurovegetative coordination, especially of cardiovascular functions. In the cat, Schomburg et al. (2003) showed sympathetic modulation of cardiolocomotor and respiratory activity with a spinopontine feedback loop extending to the hypothalamus.
Cardiorespiratory adaptation to effort involves the autonomic nervous system, particularly the hypothalamus and the pituitary gland, with regulation of blood pH, PaCO2 but also satiety and vigilance (Waldrop et al., 1986; Yeh et al., 1997). These homeostatic mechanisms, dependent on anatomically similar subcortical structures always in close relation and regulated by identical neurotransmitters, are linked to those controlling the rhythms of wake/sleep, satiety and sexuality, i.e. those involved in triggering yawning (Salin-Pascual et al., 2001; Walusinski and Deputte, 2004).
The extrapyramidal motor system has a key influence on the spinal, brainstem and cerebellar motor circuits as well as the motor cortex itself. Its neurons connect the cerebral cortex to the cerebellum, forming the corticopontocerebellar tract of the neocerebellum, whose phylogenetic development mirrored that of bipedality (Llinas and Sotelo, 1992). The cerebellum receives a copy of all motor impulses from the cerebral cortex through this tract (Schweighofer et al., 1998). This corticopontine pathway passes through the internal capsule on each side of the pyramidal tract. The lesion responsible for parakinesia brachialis oscitans is most often found at this level, involving damage to the first neuron and interrupting the corticospinal and corticonuclear pathways, but also the extrapyramidal corticostriate, corticorubral, corticonigral and corticoreticular pathways (see figure above).
At the level of the pons, the fibers form synapses in the pontine nuclei whose axons constitute the second neuron projecting to the cerebellum (middle cerebellar peduncle). The cases reported by M. Bertolotti (1905), L. Louwerse (1998) and R. Töpper (2003) show that a lesion at this level may also cause parakinesia brachialis oscitans (fig. 1).
The paleocerebellum receives signals from the spine via the dorsal and ventral spinocerebellar tracts. The two pathways transmit proprioceptive impulses from the peripheral system, i.e. from muscle spindles and Golgi tendon organs in the muscles of the limbs, trunk and diaphragm. Efferents from the paleocerebellum, after being relayed by the emboliform nuclei and the fastigial nucleus, project to the red nucleus via the superior cerebellar peduncle. In this way, the paleocerebellum controls antigravity muscles, determines the appropriate muscle tone for walking, participates in the synergistic coordination of agonist and antagonist muscles necessary for this task, all while coordinating the motor control of the diaphragm. It also sends out ascending signals which project to the centromedian nucleus of the thalamus, then to the caudate nucleus and the putamen, thereby providing a connection with the extrapyramidal system (Duss, 1998).
Like normal walking, pandiculation &endash; the generalized stretching of the trunk, limbs and diaphragm &endash; requires the uninterrupted functional activity of the corticoneocerebellospinal and the spinoarcheocerebellothalamic pathways, coupling the pyramidal and extrapyramidal control of the entire musculature.
Interruption of the corticospinal tract, whatever the etiology, causes paralysis in the arm, preventing voluntary motion. In certain cases, the cortioneocerebellospinal pathway is also interrupted. However, the proprioceptive loop conducting signals between the motor anterior spinal horn, the paleocerebellum and the lateral reticular nucleus (ventral spinocerebellar tract) remains functional. During yawning, the strong contraction of respiratory muscles represents a proprioceptive signal. An antidromic stimulation from the respiratory nuclei to the anterior spinal horn has been experimentally demonstrated in the cat (Ezure and Tanaka, 1997). It might be speculated, albeit boldly, that parakinesia brachialis oscitans is a movement of the arm (akin to the swinging coupled with respiration during walking) secondary to an incoming motor signal in the anterior spinal horn from C4 to C8, originating in the lateral reticular nucleus and traveling through the extrapyramidal pathways of the archeocerebellum (Waldrop et al., 1986).
This mechanism is consistent with the absence of movement in the leg (corticospinal interruption) and with the possibility of occurrence in the flaccid as well as the spastic phase. A preserved corticoneocerebellar pathway would prevent such a movement. Therefore, the requisite condition for parakinesia brachialis oscitans would be corticonuclear, corticospinal and corticoneocerebellar interruption, whereas the spinoarcheocerebellar pathway would remain functional. Assuming that yawning is the exteriorization of a homeostatic mechanism regulating the vigilance systems in the hypothalamus, repetitive yawning, which is frequently observed during stroke, would appear to stimulate arousal mechanisms. When a lesion in the extrapyramidal system prevents the modulating activity of the corticoneocerebellar pathway, structures that are phylogenetically more primitive may allow recovering movement in the arm during the diaphragm's maximal ampliation, as occurs during yawning.
The central nervous system in vertebrates follows a common organizational pattern and shows gradually increasing complexity with higher and higher levels of independence and functionality. The American neuropsychiatrist P. MacLean (1985) proposed a model of the nervous system's functional organization based on the study of its phylogenesis. At the base of this model is the ancestral "reptilian" brain (brainstem and basal ganglia), where yawning originates. The next level is the "paleomammalian" brain (limbic system) shared by all mammals. This is the synaptic and hormonal interface, where emotive yawning in monkeys is localized. Finally, a "neomammalian" brain comprises the top layer, characterized by cortical development in humans, particularly of the frontal lobes, where "contagious" yawning occurs (Walusinski and Deputte, 2004). If these functional levels become disconnected, as happens in certain stroke localizations, functions may reappear that are normally inhibited by a phylogenetically more recent and functionally more sophisticated structure. In this way, human pathology reveals that the coordination and regulation of body temperature, breathing, locomotion and vigilance has been perfected over time, with ever-increasing complexity and precision, from reptiles to primates.
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parakinesia brachialis oscitans
Schematic representation of the extrapyramidal tract and the localizations of lesions responsible for parakinesia brachialis oscitans. (adapted from Duus' Topical Diagnosis in Neurology, Thieme ed. 2005)