Flexor Rigidity ’ FRED A. METTLER Departments of Anatomy and Neurology, Columbia University, New York. New York

ABSTRACT Upper limb flexor pos,tures have frequently been described as part of the consequences of primate decortication, when such animals are placed in the vertical instead of horizontal position. Flexor postures have also been said by D. Denny Brown to occur following bilateral section of the eighth cranial nerve. In the present communication a pattern of alternating flexor postures (contralateral forelimb and ipsilateral hindlimb flexion with extension and magnet reaction in the ipsilateral forelimb and contralateral hindlimb) is described after postcollicular mesence- phalic hemisection. In addition, quadriflexion (flexion of all four extremities) is de- scribed following midline section of the cerebrum and mcsencephalon by a cut which, commencing with, and including, the supramammillary decussation extends back far enough to include the decussation of the brachium conjunctivum. In these experi- ments the optic chiasm, anterior commissure and rostra1 t w o thirds of the corpus callo- sum have not been cut, Severance of the decussation of the brachium conjunctivuni does not appear to be a determinative factor in the resultant flexor posture.

Although considerable emphasis has been placed upon the extensor rigidity which ordinarily immediately succeeds in- tercollicular decerebration attention to flexor rigidity has been largely confined to the consequences of cord transection. Ex- ceptions to this are studies of the copula- tory position in spinal animals, upper limb flexor postures in high spinal transection in man and Fulton’s (’49, p. 154) state- ment that flexion “is also seen in certain cerebral diplegias, but here the mecha- nism is not entirely manifest except that the pyramidal system on both sides must be destroyed.” The present communica- tion is concerned with placing on record another condition in which flexor rigidity appears and which has no clear causal relationship with interruption of any of the commonly accepted components of the pyramidal system either in the spinal cord or elsewhere.

Before presenting data demonstrating that flexor rigidity succeeds midline sec- tion of the diencephalic and mesencephalic commissures (for this it is which produces the flexor state with which I am principally concerned) it is necessary ( a ) to explain my understanding of rigidity and (b) to direct attention to three features of the current literature on decerebrate rigidity itself with a view to establishing that flexor rigidity also has been encountered in that

condition. Definition. By rigidity I refer to resistance on the part of the muscles of a joint to gentle, slow efforts to move the joint passively. I do not consider rigidity quite synonymous with spasticity, which I take to be overactivity of the myotatic re- flexes and which may or may not be present in rigidity. In rigidity (in contrast to spasticity) the activity of the muscle precedes the external adventitious brisk stretch stimulus by means of which deep reflexes are commonly evoked. Such em- phasis appears to be necessary since a distinction is not always drawn between spasticity and rigidity. According to Bard (’56, p. 1059) spasticity is what is ob- served in the stiff hemiplegic limb, and this is the equivalent of decorticate rigid- ity. Ruch’s (Ruch and Fulton, ’61, p. 271) distinction between spasticity and rigidity employs the occurrence of the lengthening or claspknife reaction in the former. Ac- cording to Houssay (’55, p. 1023) rigidity is simply an exaggeration of the myotatic reflexes. Magoun and Rhines (’47, p. 3 ) aver that “increased resistance to manipu- lation, hyperactive deep reflexes; and clonus - together constitute spasticity.” It is no longer possible to identify rigidity as Denny-Brown does (’60, p. 786) with increased discharge of the small-fibered

1 Aided in parb by N.I.H. grant NE 05184-01.

383 J. COMP. NEUR., 125: 383-392.

384 FREI) A . METTLER

gamma system since there is no such dis- charge when rigidity is produced by the anemic decerebration technique (Granit, '57). For present purposes I shall follow Hoefer ('41 ) and Hoefer and Putnam ('40) who use the character of the electromyo- gram as the critical distinguishing feature between spasticity and rigidity. In the former condition there is no appreciable degree of electromyographic activity in the muscle until it is proprioceptively activated. In my experience spasticity, such as is experimentally produced by relatively pure and complete pyramid sec- tion has the following character. Slow, passive movement of the limb is not re- sisted but the myotatic reflexes have a low threshold, large amplitude, rapid re- sponse and exhibit a widened reflexoge- nous zone. In the rigidity which follows hemidecerebration, on the other hand, there is a definitely elevated background of innervation of variable intensity, while the individual is awake and without any necessary apparent change in propriocep- tive inflow. The muscle resists slow pas- sive movement and the response of the proprioceptive reflex while often en- hanced, may be difficult to detect because of the sustained state of muscular con- traction (Nlagoun and Rhines, '47; see fig. 11). Spasticity is, as Denny-Brown has observed, a condition of heightened myotatic reflex responses. Briskly stretch- ing a muscle elicits spasticity but slow lengthening does not. In rigidity slow, as well as rapid, passive movement is op- posed and the opposition does not fall away in the form of a reflex jerk or clonus, but continues as a specific quantum.

Difficulties in relating the experimental literature on decerehratiorz to conditions of clinical rigidity. The three features of the literature referred to above are: (1) what is commonly taught on this subject in courses on physiology in medical schools is of restricted value in dealing with many, if not most, of the problems with which the clinician is routinely con- cerned, ( 2 ) the decerebrate state is by no means invariably, one of consistent and enduring antigravity extension and ( 3 ) the didactic literature on the subject of decerebration leaves something to be de-

sired with regard to ( a ) accuracy and (b) consistency.

With regard to the first point it is, I suppose, evident that the clinician's chief concern is with rigidity in general, and not exclusively with that specific form of rigidity (i.e. decerebrate rigidity) which is the primary interest of the professional physiologist. Indeed, the latter's observa- tions are often restricted to the acute phenomena of decerebrate rigidity. The results of the effort to employ such ma- terial, within a clinical frame of referencc, often do not repay the labor involved.

As implied at ( 2 ) above, the term de- cerebrate rigidity may be used for condi- tions which are by no means identical. Not only are animals prepared by the various techniques of decerebration - guillotine, anemic, surgical (with or with- out removal of tissue rostra1 to the cut) - different, but differences are also en- countered among animals produced by the same technique. If all one is interested in is the production of an insensitive preparation, suitable for studying the pe- ripheral neural system or cardiovascular reflexes, one is not likely to be concerned with inconsistencies due to disturbances short of vascular collapse, or respiratory failure, but the practical neurophysiologist cannot help but be distressed by pheno- mena such as cerebellar hemorrhage, sub- tentorial tamponade and enormous swell- ing of the brain. Further he must give attention to the precise level and angle of the section when a cutting technique is used. Theoretically the condition of de- cerebrate rigidity is uniform but in practice one encounters variations between acute and chronic decerebrate rigidity, extensor and flexor decerebrate rigidity (which may be a surprise to those accustomed to think of decerebrate rigidity as invariably exten- sor) and high and low decerebrate rigidity. We cannot know what an author means when he speaks of decerebrate rigidity, without further qualification, and we still cannot be certain about what he really ob- served unless he publishes his protocols. It is a parlous practice to assume that when decerebrate rigidity is spoken of extensor ripdity is meant. Indeed, since much of the literature is limited to acute experi- ments, a particular author may not him-

FLEXOR RIGIDITY 385

self have known whether the condition he studied is enduring or not or. if enduring, to what degree. What the clinician is con- cerned with are however, by and large, en- during phenomena.

Fulton’s reference to cerebral diplegia, and Bards comment reminds us that de- corticate rigidity must not only be distin- guished from decerebrate rigidity but that the effect of unilateral lesions i s different from bilateral. Removal of one motor area, or all of the cerebral cortex from one hemisphere, produces a perceptible, albeit mild, degree of rigidity (Mettler, ’43). The result differs from decerebrate rigidity in that (a) it is characterized by resistance to passive extension of the extremities and not to flexion, and (b) the rigidity is not so pronoiinced as the extensor rigidity one encounters when the neuraxis is hemi- sected between the small- and large-celled parts of the red nucleus. On the other hand. removal of both motor areas in a primate. or bilateral decortication, produces ( a ) very much more rigidity than succeeds uni- lateral decortication and ( b ) in certain circumstances it is extensor and not flexor (in cats and dogs, for example (Bard. ’56. p. 10571, and (Mettler, ’44b, pp. 105-106) in primates in the horizontal position).

Discrepancies in the literature on postuie in decorticate and

decerebrate rigidity Fulton’s picture of decerebrate rigidity is

not only difficult to verify but, occasionally, apparently at odds with his sources. For example he states that when “the cere- bral hemispheres are removed by prepon- tine section of the brain stem” an exten- sor rigidity develops and “continues with- out intermission for days.” “From the more recent observations of Bazett and Penfield it is clear that the rigidity of the decerebrate state persists indefinitely.” (Fulton, ’38, pp. 150-151; ’43, pp. 144; ’59, p. 158). As noted, this material appeared in all three editions of Physiology of the Neruous Sys tem. Bazett and Penfields data do not support the statement Fulton rests on their authority, as will be noted below. Fulton also states, following Sher- rington, that in semidecerebration, the re- sultant unilateral rigidity is ipsilateral (Fulton, ’38, p. 151; ’43, pp. 144-145; ’49,

pp. 158-159). This statement has been car- ried forward in Ruch and Fulton’s Medical Physiology and Biophysics (’61, pp. 206- 207). Doubt about the 1,alidity of this Sher- ringtonian proof of the assumption that decerebrate rigidity is of extrapyramidal origin was raised long ago by Thiele (’05), and Bazett and Penfield (’22) nullified the Sherringtonian argument by demonstrat- ing that ipsilateral rigidity (when it oc- curs) shifts to the opposite side by the third postoperative day. They argued. in fact. that such ipsilateral rigidity is the result of irritation and not release. Some of Bazett and Penfield’s animals exhibited flexor instead of extensor rigidity and if one attempts to correlate this appearance of flexor rigidity with the level of decere- bration one is struck by the fact that the number of animals which fulfill the three conditions necessary for forming such an opinion (a, survival beyond 4-5 days, b, an intelligible description of the physio- logic condition of the animal, (with or without infection) and c, verification of the level of section) is rather small. Moreover, of the descriptions of the approximately eight animals that one can visualize, true extensor rigidity seems to have appeared and continued uninterruptedly in only two. One of these had a supracollicular section and the other a n infracollicular. Flexor rigidity appeared in three cases with le- sions in mid-and infracollicular levels. Flaccidity occurred in one animal and running and struggling movements in two animals with sections at the same levels. The overall picture is one of a highly vari- able situation in which initial extensor rigidity tended, after 3-7 days, to lessen or disappear or be interrupted by other situ- ations such as flexor rigidity, flaccidity or, more commonly, poorly adaptive or strug- gling activity. It has not been possible for me to detect any correlation between any of these conditions and the rather irregu- lar deprivations described by Penfield (who did the morphologic study). Thiele (’05) had previously noted that flexor rather than extensor rigidity might appear in the acute decerebrate and Bazett and Penfield at- tempted to grapple with this problem as it appears in the hemidecerebrate.

Here they were confronted with a new and unexpected difficulty - the nature of

386 FRED A. METTLER

the rigidity shifted sides (in their appar- ently only chronic case of precollicular hemisection) after the second day. In ani- mals with cuts at lower levels the problem was even more complicated. They seem to have had only four such additional cases and only one of these apparently lived be- yond four days. It is difficult to recon- struct the results since the full protocols are not given and the data were quite variable. Bazett and Penfield were appar- ently unable to organize this material very satisfactorily and although they were fa- miliar with Thiele’s paper on the subject they do not seem to have considered seri- ously his specific conclusion that the tract which causes unilateral “rigidity decus- sates anterior to the decussation of the superior cerebellar peduncle.” Thiele had also stated that the acute homonymous unilateral decerebrate rigidity such as Sher- rington had described might be due to ir- ritation of the superior cerebellar pedun- cle. Bazett and Penfield do observe that Thiele had noted that when the hemide- cerebration is in the tectal area (i.e., more rostrally) the unilateral decerebrate rigid- ity is contralateral but they did not em- phasize that their results did not agree with his. The acute unilateral extensor rigidity which they found to be homolateral oc- curred after pretectal hemisection where- as his followed low hemisection and with a lesion such as they describe he got a contralateral effect. Decerebrate rigidity, he thought, was due to deprivation of a “thalamic” influence which “is transmitted along a tract which decussates high up in the mesencephalon.”

Since the number of reported detailed experimental studies on chronic decere- brate (not decorticate) animals can be counted on the fingers of one hand (Bazett and Penfield, Keller (’45) and Bard - and their associates) it is obvious that it is un- wise to fail to give them detailed and care- ful consideration.

The flexor posture We have seen then, in the material dis-

cussed above, that in addition to the flexor posture frequently encountered in com- plete cord transection, such postures may appear in the decerebrate animal and may be encountered in certain positions of de-

corticated primates. It is not unusual to find that the predilection posture of the hemiplegic, or the flexor posture of the diplegic, is explained upon the basis of pos- tural alteration of the decerebrate state but the rationale of Fulton’s statement quoted on page 383 cannot be reconciled with what we know about the absence of rigidity following pyramid section. Fulton (’49, p. 414, et seq.) himself quotes the evidence on the latter point but does not appear to have realized that this was inconsistent with what he said earlier in his book. Since we know that the cortex emits ex- trapyramidal projections it might be pos- sible to rationalize Fulton’s comment about diplegia by substituting the word extrapyramidal for pyramidal. It then be- comes necessary to ask to what extrapy- ramidal mechanism we are referring. There is no experimental evidence to sup- port the conjecture of neuropathologists that pallidal lesions, which do not en- croach upon pyramidal projections, release any high order of rigidity and the evidence that such a phenomenon succeeds nigral damage is far from conclusive (Mettler, ’64). Neither are we aware of the descrip- tion of the precipitation of an extensor posture by any supramesencephalic lesions which quite spare the cortex and its pro- jections. We are also still a long way from a clear understanding of the decerebrate situation - particularly hemidecerebra- tion. We have seen that a Sherringtonian error, which has been known to be a mis- take for over a quarter of a century is still uncorrected in texts written by persons with the reputation of personal authority in the field and it is of some interest to observe that some aspects of hemidecere- bration have remained quite undetected. One of these is the crossed flexor-exten- sor posture of primate infracollicular hemi- section. Figures 1-4 show the effects of a right-sided operation (animal 3272) one day after operation. For our present pur- pose the interesting feature of such ani- mals is the presence of flexion in this fixa- tion of the normal locomotor pattern of crossed flexion-extension,

A more impressive flexor pattern can be elicited by division of the deep commissural systems of the brain. The posture of one such animal five days after operation is

FLEXOR RIGIDITY 387

Figs. 1 4 Position of animal 3272, two days after right postcollicular hemisection.

shown in figures 5-8 and its protocol is given herewith.

Animal 3278, a pig-tail rhesus was subjected on April 15, 1964 to exposure of the dorsal aspect of the mesencephalon following retraction of the left occipital lobe and severance of the tentorium cerebelli. A dulled razor blade template was in- serted through the dorsum of the mesencephalon, ventrally along the midline.

On the day after operation the animal lay on its abdomen with all the extremities flexed. The head was turned toward the left and the animal tended to roll toward the left side and to rotate counterclockwise on the floor. The eyes were in a neutral conjugate position and showed no move- ment except vertical nystagmus of small ampli- tude. The right palpebral fissure was narrower than the left. Both extremities exhibited an ex- cellent grip. An object offered to the hand was promptly seized and bitten.

Placed on the horizontal bar (figs. 5-8) all extremities were strongly flexed and resisted ex- tension. There was a tendcncy to turn toward the left so that there was some convexity of the spine toward the right.

Placed in the seated position in the examining chair the legs were adducted with the knees knocking together (see also fig. 9 ) . Both legs were flexed and resisted extension. The patellar reflexes were brisk, prompt and of small ampli- tude. The left plantar response was extensor, the right sole was silent. There was no evident ataxia.

On April 20th motion pictures were made of the above phenomenon. It was observed that the riqht pupil was slightly larger than the left. While the right cye was not moved, the left showed slight lateral activity to the left of the midline only. The animal was able to sit up in a shaky position of forward flexion. All the limbs continued in the flexed posture. The right arm was well used in monomanual feeding. The left participated in a clumsy manner. No ataxia could be dctected. Neither plantar response could be elicited. The patellar reflexes were extremely ab- normal. The reflexogenous zone was very nar- row. the response very rapid and the leg flexors almost immediately contracted reducing the am- plitude of the reflex to a very narrow range.

O n April 21st the animal was able to sit up somewhat better but its extremities were drawn

388 FRED A. METTLER

Figs. 5-8 Position of animal 3278, five days after midline section of the diencephalon and mesencephalon (through the posterior third of the corpus callosum) and involving the supramanimillary decussation, decussation of the brachium conjunrtivum and intervening decussations, and commissure.

up and since it continued in a flexcd bodily pos- ture there was considerable difficulty in main- taining balance. Upon moving it tended to fall over backward but it caught itself with either hand before hitting the floor. Startling the ani- mal with a sudden loud noise produced falling. The right hand was used more effectivcly than the left which was commonly kept in the flexed posture with the knuckles in contact with the bars of the cage instead of grasping them. Fre- quently the animal sat with the elbows flexed and the forearms elevated directly in front of the body (held out in the air, see fig. 9). In such a position the left but not the right hand some- times exhibited a fine fast tremor. No tremor was apparent when the hands rested on objects. The right upper extremity behaved differently from the left in another respect. It exhibited a kind of motor restlessness in which it was picked up at intervals of about every 15 seconds and replaced (for example, on the cage door) or held momentarily in the the air.

On April 23rd the animal was observed to ex- hibit a type of movement in which it turned its head over the right shoulder at which time the occiput would move backward, the eyes upward and thc animal then fell over backward. The left arm was still not used preferentially in fceding and the right arm occasionally exhibited a rotatory tremor when holding food.

On April 27th motion pictures were taken. The flexor posture and counter-clockwise turning continued. The flexed right arm was often held in the air somewhat to the right of the body. The flexed left foot was often held off the ground.

The episodes of slow hand retraction and back- ward falling had become more frequent. A fine tremor was now evident not only in all four ex- tremities but also in the musculature of the body. This tremor was complex consisting of a fine, very fast, small amplitude component which was superimposed on the basically slower component of large amplitude. Gross ataxia was now appar- ent during feeding movements of either hand. The right continued to be preferred. A peculiar feature of this abnormality was the fact that, upon occasion, the animal would employ the left extremity for monomanual feeding without any particularly noticeable ataxia. The patellar re- flexes continued fast and tight but the left was looser than the right. The threshold of the left was lower and its amplitude was larger. The plantar response was sluggish on the left. On the right there was a suggestion of dorsiflexion of the toes but not hallux. No fanning occurred.

In the next two weeks there were no further changes in the animal. In the cage it was found to spend most of its time clinging to the wire on the side after having ascended as far as it could go. (Such behavior is a feature of monkeys that maintain flexor postures and that have paralysis of downward gaze.) The eyes were never seen to be moved downward or to the right in conjugate fashion. Left lateral conjugate gaze was noticed and was better in the left eye. If the animal was placed in a cage with smooth plastic walls it tended to back up in such a way that its back and sides were supported in a corner. The fine rapid tremor continued. The animal was dis- patched on May 7th.

FLEXOR RIGIDITY 389

Figs. 9-12 Animal 3278 (see legend to figs. 5-8) shown in a retropulsive episode 12 days after operation. In figure 9 the monkey is sitting in the right rear corner of the plastic box and beginning to move. In figure 10 he has pushed directly backward and in figure 11 he is undergoing a fall back- ward from which he recovers by backing up into the left rear corner of the box.

Autopsy disclosed no notable occipital traumd (the right posterior superior cerebral veins were, of course, divided and the great cerebral fissure diverged toward the right). The posterior part of the corpus callosum was severed as far forward as the posterior commissure which was severed by a right paramedian section which extended into the tegmmtum of the pons and rostrally it terminated in the subthalamic decussation.

Features of particular interest for the clinician are the phenomenon resembling oculogyric crisis and the retropulsion (syn- drome of Hermann H. Hoppre, vide Claude and Levy-Valensi, p. 181, ’22) such ani- mals display. Such phenomena are, of course, well known and were accurately commented upon by Muskens (’22) (“Clinical and physiological observations lead us to suppose that structures ex-

ist in the mesencephalon, near the raphe, and ventral to the posterior longitudinal bundle, lesions of which cause falling back- wards and deviation of the eyes upward,” p. 477). The precise nature of the mecha- nism referred to by Muskens still does not appear to have been identified. I have not found anything conclusive on the matter and Professor Morris Bender tells me that he is also unaware of the precise structural substrate of the phenomena which he is inclined to attribute to damage of more than one single system. In his view the damage must be of such a nature as to disrupt a considerable number of mecha- nisms all of which are of utility in correlat- ing visual clues from the two sides. It is a

390 FRED A. METTLER

Fig. 13 Norma dorsalis of brain of animal 3278. Attention is called to the absence of any involvement of the motor cortex. The approach to the interior of the thalamus was made by retracting the right occipital lobe, after cutting the right superior cerebral veins which traverse it, and severing the caudal part of the corpus callosum (that part lying behind the posterior commissure) .

matter of considerable interest, I believe, that there does not appear to be any indica- tion that the psychologists who report upon what have been rather enthusiastically called “split-brain” preparations, have en- countered this phenomenon or, if they have, have recognized it. In general the so- called “split-brain” psychological literature eschews early description and in spite of the rather definitive position taken by an authority like Sperry, about what has been cut in the monkeys his associates are said to have prepared and with which they would seem to have worked (see the illus- tration on pp. 44-45 in Scientific Ameri- can, January, 1964), it is very difficult to obtain a clear account, either from the lit- erature or discussions, of the fundamental

neurologic status and basic morphologic condition of the brains of such monkeys. Neither have I been able to find, in the lit- erature of such work, any account of the flexor posture shown in the photographs presented herewith nor have I, by ques- tioning, been able to discover that it has been noticed.

It is apparent that it is a matter of con- siderable importance to determine the min- imal mechanisms section of which pro- duces generalized flexor rigidity. A wide range of material including severance of practically all of the commissural systems simply by paramedian lesions is available but damage of no single system appears to yield the flexor posture any more than dam- age of any single system produces decere- hrate extensor rigidity. Apparently the suhthalamic decussation (in the vicinity of which the extensor plantar phenomenon shifts sides, Mettler, ’44a) and/or poste- rior commissure must be included in the lesion.

LITERATURE CITED

Bard, P. 1956 Medical Physiology. St. Louis, The C . V. Mosby Co.

Bazett, H. C. , and W. G. Penfield 1922 A study of the Sherrington decerebrate animal in the chronic as well as the acute condition. Brain, 45: 185.

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Hoefer, P. F. A. 1941 Innervation and “tonus” of striatal muscle in man. Arch, Neurol. and Psychiat. (Chicago), 46: 947.

Houssay, B. A. 1955 Human Physiology. N. Y., McGraw-Hill.

Keller, A. D. 1945 Generalized atonia and pro- found dysreflexia following transection of the

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