case report - oxford academic

Medial Pontine Hemorrhagic Stroke

Background and Purpose. This case report documents a rare opportu-nity to observe the motor function of an individual for nearly 6 monthsfollowing a primary pontine hemorrhage in the medial pontinetegmentum of the brain stem. The purpose of this report is to illustratehow knowledge of the location of the hemorrhage, in conjunction withknowledge of brain-stem structure-function relationships, informsphysical therapist examination and intervention. Case Description.RM, a right-handed 81-year-old man with hypertension, had a hemor-rhagic brain-stem stroke that severely compromised control of postureand whole-limb movements. Some residual ability to use the right handand fingers remained, provided the trunk and right upper arm werestabilized. RM had undiminished intellectual abilities and unalteredmemory because of sparing of cerebral cortices. RM’s cognitive abili-ties, however, were obscured by severe impairments in interpersonalcommunication because of extensive damage to cranial nerve struc-tures. Computed tomographic scans verified that the hematomacrossed the midline and was confined to the medial pontine tegmen-tum. Discussion. We interpret motor deficits resulting from stoke in themedial pontine tegmentum in terms of damage to brain-stem descend-ing motor systems and ascending somatosensory systems. Recognitionof cognitive and residual motor abilities following brain-stem strokecan aid in the development of rehabilitation strategies. [Ruhland JL,van Kan PLE. Medial pontine hemorrhagic stroke. Phys Ther.2003;83:552–566.]

Key Words: Brain-stem stroke, Descending motor systems, Motor rehabilitation, Neural control of

movement, Primary pontine hemorrhage, Quality of life.

Janet L Ruhland, Peter LE van Kan

552 Physical Therapy . Volume 83 . Number 6 . June 2003

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Recent autobiographies of people who havesurvived a brain-stem stroke illustrate theunique challenges they face.1–3 Often, peoplewith brain-stem stroke are left with their cog-

nitive abilities fully intact, but with an inability to controlmovements of their body. In contrast, strokes that affectcerebral cortices (or their output fibers in the internalcapsule) often result in both cognitive and motorimpairments. This case report documents motor impair-ments of an individual following a primary pontinehemorrhage bilaterally in the medial pontine tegmen-tum of the brain stem. This case is unique because mostindividuals with lesions in this location do not survive, orthey remain unconscious. A review of neuroanatomic,neurophysiologic, and pathophysiological studies ofdescending motor pathways and clinical manifestationsresulting from brain-stem versus cerebral cortical strokeprovides the background and support for the motordeficits described in the case report. The case reportemphasizes the importance of taking into account thelocation of the lesion and known structure-functionrelationships in the clinical management of people withbrain-stem stroke.

Functional Organization of Descending MotorSystemsThe now classic studies of the Dutch neuroscientistKuypers and colleagues4–7 have provided a conceptualframework for functional organization of descendingmotor pathways. The studies demonstrated that cerebralcortical motor areas and brain-stem nuclei in nonhuman

primates give rise to descending motor pathways that arefunctionally distinct. Kuypers classified brain-stem motorpathways into medial and lateral systems. The medialsystem includes the reticulospinal, vestibulospinal, inter-stitiospinal, and tectospinal tracts, which originate fromthe medial reticular formation, the vestibular nuclei, theinterstitial nucleus of Cajal, and the superior colliculus,respectively. Medial-system pathways project bilaterally,via ventral columns, to ventromedial regions of theventral horn where motoneurons for axial and proximalmuscles are located. The lateral system includes therubrospinal tract, which originates from the red nucleus.The rubrospinal tract projects contralaterally, via lateralcolumns, to dorsolateral regions of the ventral hornwhere motoneurons for distal muscles are located. Cere-bral cortical motor areas influence spinal circuitrydirectly via corticospinal tracts and indirectly via medialand lateral brain-stem systems. The ventral corticospinaltract projects, via ventral columns, to ipsilateral spinalcord segments and then terminates bilaterally in ventro-medial regions of the ventral horn. The lateral cortico-spinal tract projects contralaterally, via lateral columns,to dorsolateral regions of the ventral horn, where itsterminations largely overlap those of the lateral brain-stem system. Based on the combined evidence of neuro-

JL Ruhland, PT, MA, is Staff Physical Therapist, Meriter Health Center, Madison, Wis, and a graduate student in the Department of Kinesiology,University of Wisconsin–Madison, Madison, Wis.

PLE van Kan, PhD, is Associate Professor, Department of Kinesiology, Room 3195, Medical Sciences Center, University of Wisconsin–Madison,1300 University Ave, Madison, WI 53706-1532 (USA) ([email protected]). Address all correspondence to Dr van Kan.

Ms Ruhland and Dr van Kan provided concept/project design, writing, data analysis, project management, and facilities/equipment. Ms Ruhlandprovided data collection.

This article was submitted August 15, 2002, and was accepted January 11, 2003.

Knowledge of brain-stem anatomy

and pathophysiology is important for

recognizing patients’ remaining

cognitive and motor abilities following

brain-stem stroke.

Physical Therapy . Volume 83 . Number 6 . June 2003 Ruhland and van Kan . 553

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anatomic and behavioral observations, Kuypers con-cluded that the medial brain-stem system is the basicmotor system upon which controls exerted by cerebralcortical motor areas and the lateral brain-stem systemare superimposed.7

Studies conducted over the past 3 decades have providedample evidence in support of Kuypers’ view of descend-ing motor pathway organization. All major componentsof the medial brain-stem system, for example, contributeimportantly to control of posture and whole-body move-ments. Vestibulospinal fibers in the medial longitudinalfasciculi (MLF) project to extensor and lateral neckmotoneurons and, together with interstitiospinal projec-tions, function to stabilize the head in space.8,9 Vestibulo-spinal fibers from the lateral vestibular nuclei exciteipsilateral extensor motoneurons of the limbs andtrunk,10 and they are important for maintaining uprightposture and for extending the limbs when falling.8Reticulospinal neurons receive input from varioussources, including peripheral afferents and the superiorcolliculus, vestibular and deep cerebellar nuclei, andcerebral cortical motor areas.11 The medial reticulo-spinal system contributes to the control of behaviors thatinvolve synergistic activation of broad groups of muscles,such as neck and vestibular reflexes, orienting responses,and locomotion.11–13 Tectospinal fibers originate fromlarge cells in deep layers of the superior colliculus,14

which are important for orienting the eyes, head, andtrunk to visual, auditory, and somatosensory stimuli.15,16

Thus, the medial system provides the basic control ofposture and whole-body movements upon which cere-bral cortical motor areas organize more highly differen-tiated movement (eg, for integrating voluntary limbmovements with posture in cats12 and for control ofrelatively independent finger movements in pri-mates6,17–19). The lateral system preferentially influencesdistal muscles20–23 and provides control of voluntarymovements of the arm, hand, and fingers for reachingand manipulating objects in primates5,22,24–26 and forcontact placing27,28 and for limb trajectory and footplacement during locomotion in cats.13,29–32

In summary, a large body of work has firmly establishedthe basic functional organization of descending motorpathways. In addition, recent findings have providedsignificant new insights in the contribution and func-tional overlap of different descending pathways impor-tant for the control of multijoint, coordinated move-ments such as locomotion and reaching to grasp andhave provided new perspectives on Kuypers’ classic viewof descending motor pathway organization.

Brain-Stem Versus Cortical StrokePeople with brain-stem stroke are a minority of a largergroup of people who have sustained strokes. Stroke is

one of the leading causes of adult disability and is ournation’s third leading cause of death behind heartdisease and cancer.33 Each year, more than 750,000Americans have a first or recurrent stroke,34 resulting inan age-adjusted mortality rate of 25.1 deaths per 100,000people in the population in 1998.33 In a recent study,35

83% of strokes were ischemic, 10% were intracerebralhemorrhages, and 7% were subarachnoid hemorrhages.Many fewer people have brain-stem stroke as comparedwith cortical stroke. Primary pontine hemorrhage, forexample, accounts for less than 8% of incidences ofintracerebral hemorrhage (7.5%, 50/667 cases over aperiod from 1935 to 196436; 7.9%, 61/771 cases over aperiod from 1985 to 199037). Moreover, brain-stemstroke is associated with a much higher mortality rate ascompared with cortical stroke because ascending anddescending projections from the reticular formation andvital cardiovascular and respiratory centers are located inthe brain stem. Primary pontine hemorrhage, for exam-ple, is highly fatal, with overall case mortality rates ashigh as 61%37 to 75%.36 The prognosis of primarypontine hemorrhage, however, depends on the size,location, and extent of the hematoma. Bilateral lesionsinvolving the medial pontine tegmentum were a minor-ity of cases (14%, 7/50 cases36; 11.5%, 7/61 cases37) andhad the lowest case survival rates (0/7 cases, survival2–10 days36; 14.3%, 1/7 cases37). Furthermore, brain-stem strokes are frequently abrupt in onset and producecoma, which precludes study of associated motor defi-cits. Coma is especially common following bilaterallesions that involve the medial pontine tegmentum.38

Because of low survival rate and poor prognosis, fewpeople with brain-stem stroke enter rehabilitation, andmost accounts of motor deficits and rehabilitation fol-lowing stroke concern people with cortical stroke ratherthan brain-stem stroke.

Clinical manifestations following cortical stroke andbrain-stem stroke differ. Following stroke in cerebralcortices (or their output fibers), people often exhibithemiplegia or hemiparesis, upper motor neuron facialweakness, hemi-somatosensory loss, and loss of vision inone hemifield.39,40 Weakness and somatosensory loss aremost prominent on the side of the body contralateral tothe damaged cortex, and typically distal muscles aremore strongly affected than proximal muscles.41 Higher-level perception and cognition also may be deficientfollowing a cortical stroke, depending on which regionsof the cerebral cortex are damaged. Stroke of thedominant hemisphere, for example, frequently results inaphasia,42 whereas stroke of the nondominant hemi-sphere frequently results in anosognosia and contralat-eral hemineglect.43 Following brain stem stroke, coma ordeath are common. If a patient does survive, a seeminglysmall lesion often has devastating consequences becausemany nuclei and neural pathways, including cranial

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nerve nuclei, descending motor pathways, ascendingsomatosensory pathways, and widespread ascending anddescending projections from the reticular formation, aredensely packed in the brain stem. Motor deficits andsigns following brain-stem stroke may include contralat-eral hemiparesis and ipsilateral lower motor neuronfacial weakness or sensory loss.44,45 Motor deficits follow-ing brain-stem stroke, however, also may be bilateraland, depending on the extent and location of damage,may include one or several of the following signs:quadriplegia, pupillary changes, diplopia, gaze palsies,internuclear ophthalmoplegia, dysphagia, dysarthria,vertigo, and ataxia.44,46–48 Following cortical stroke, axialand proximal limb muscles often remain relatively morefunctional than distal muscles because the corticospinalsystem primarily innervates distal musculature. In con-trast, a brain-stem stroke may result in the reversesituation. That is, following a brain-stem stroke, controlof axial and proximal limb musculature may be severelyaffected, whereas control of distal musculature may berelatively more spared.

The neural bases underlying therapy-induced improve-ments in motor function following stroke are, at present,incompletely understood. A large body of evidence fromneurophysiologic, neuroanatomic, and neuroimagingstudies in animals and humans supports the view thatcerebral cortical circuitry is highly plastic.49–51 The dem-onstrated plasticity in neuronal circuitry may provide ascientific basis for commonly used therapeuticapproaches following cortical stroke. For example, tech-niques such as constraint-induced movement thera-py52–54 and repetitive rehabilitative training of theimpaired limb55,56 are thought to promote functionalreorganization following neuronal damage. In addition,robot-aided neurorehabilitation reduces impairmentand has a positive effect on reorganization of the adultbrain by concomitantly controlling the amount of ther-apy delivered to a patient and measuring the patient’sperformance.57,58 Furthermore, transcranial corticalstimulation,59 cognitive rehabilitation,60,61 neuromuscu-lar stimulation,62,63 biofeedback therapy,64,65 and motorimagery66 are all based on the idea that sensorimotorstimulation will enhance cortical reorganization follow-ing injury, thereby improving motor function. Althoughmuch less is known about plasticity of brain-stem cir-cuitry and use-dependent reorganization of neural cir-cuitry following brain-stem stroke, current therapeuticapproaches following brain-stem stroke are similar tothose following cortical stroke (eg, Hummelsheim andEickhof67). Clearly, a more refined understanding of theneural bases underlying cortical and brain-stem strokesis needed to optimize physical therapist examinationand intervention.

Our case is an excellent one to study the uniquemanifestations of a brain-stem stroke and the interven-tion considerations required. The case exemplifies acognitively, socially, and emotionally intact individualwith extremely limited motor abilities who needed spe-cial consideration.

Case Description

Patient History“RM” was a right-handed 81-year-old man with hyperten-sion and poorly controlled atrial fibrillation that wasmanaged with anticoagulant medications on a long-termbasis. He was doing quite well until the morning of theday he was admitted for emergency care with headache,diaphoresis, dizziness, diplopia, sudden onset of rightarm tingling, numbness, and weakness, followed byprogressive slurred speech. Computed tomographic(CT) scans of the head showed progressive hemorrhagicstroke intrinsic to the pontine tegmentum of the brainstem, with rupture into the fourth ventricle (Fig. 1A).The observed signs of damage to cranial nerve structuresand ascending somatosensory pathways are summarizedin the Table. Pupils were equal in size and reactive tolight. Horizontal eye movements and conjugated gazewere severely restricted as a result of bilateral abducentnerve paralysis. Vertical eye movements were normal.The jaw was deviated to the right. He showed bilateralfacial weakness (right greater than left) and difficultieswrinkling the forehead and closing the eyelids. He hadsevere dysphagia. His oral pharynx was dry. His tongueand palate moved normally. His gag reflex was good.Respirations were of the Cheyne-Stokes type. Tactilediscrimination and sensation of position of limbs wereimpaired on the left and intact on the right. A distortedand heightened reaction to noxious stimuli was notedon the left. Bilateral segmental static reflexes (eg, flexorwithdrawal and crossed extension) were present. Deeptendon reflexes were decreased. Extensor plantarreflexes (Babinski sign) were negative. Automatic laby-rinthine and neck reflexes were greatly impaired orabsent. Although RM was oriented, attentive, and coop-erative, his level of arousal fluctuated. At times, he wassomnolent and difficult to arouse. Verbal expression wasdifficult due to dysarthria. Audition and oral compre-hension were normal, and no aphasia or signs of cogni-tive impairment were evident.

RM’s movement dysfunction, described in detail below,became progressively more evident over the first few daysfollowing the stroke. Upon stabilization of his condition,he was unable to walk, stand, or sit upright. Althoughsome ataxia of the left upper extremity was noted, he didnot develop dysmetria, dysdiadochokinesia, intentiontremor, or asynergia. He showed good judgment con-cerning his functional limitations. Post-stroke depression


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Figure 1.Location and extent of RM’s hemorrhagic stroke. (A) Head computed tomography (CT) scan showing the extent of hemorrhage in the medial pontinetegmentum of the brain stem (arrow). Abbreviations: IV�fourth ventricle, CB�cerebellum. (B) Placement of a section through the sella turcica and thecaudal third of the fourth ventricle that corresponds to the plane of the CT scan in panel A and the histological section in panel C. The plane of section(thick line) is at a 25-degree angle with respect to the horizontal stereotaxic plane (thin line). (C) Histological section in the plane of the CT scan inpanel A. The superimposed white lines indicate the extent of hemorrhage reconstructed from 2 successive CT scans. The broken white line correspondsto the CT scan in panel A; the solid white line corresponds to a CT scan at a level 6 mm superior to that of the CT scan in panel A. Abbreviations:AbdNu�abducent nucleus, AbdNr�abducent nerve roots, CTT�central tegmental tract, CST�corticospinal and corticobulbar tracts, FacNr�facialnerve, FacNu�facial nucleus, ForVen�fourth ventricle, LL�lateral lemniscus, LVN�lateral vestibular nucleus, MCP�middle cerebellar peduncle,ML�medial lemniscus, MLF�medial longitudinal fasciculus, PonNu�pontine nuclei, PonRet�pontine reticular formation (inferior part), RaNu�raphenuclei, RST�rubrospinal tract, SL�spinal lemniscus (spinoreticular, spinotectal, and spinothalamic tracts), SONu�superior olivary nucleus,SpTTr�trigeminal nerve spinal tract, SYNu�superior vestibular nucleus, TecSp�tectospinal tract, TrapB�trapezoid body, TriMoNu�trigeminalmotor nucleus, VesCochNr�vestibulocochlear nerve roots. The diagram in panel B is reproduced with permission from Hanaway J, Scott WR, StrotherCM. Atlas of the Human Brain and the Orbit for Computed Tomography. St Louis, Mo: Warren H Green Inc; 1977. The histological section in panelC is provided courtesy of the Digital Anatomist Program of the Department of Structural Anatomy of the University of Washington.


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was treated with antidepressant medication (Zoloft,*100 mg/d). Over the next few months, RM developed agross, low-frequency, rest and intention tremor of thehead, neck, trunk, and left extremities, termed “Claudesyndrome” or “rubral tremor.”68,69 Approximately 6months following the initial stroke, RM had anotherstroke and died of pneumonia.

ExaminationClinical findings were obtained from emergency depart-ment, hospital, and nursing home records; from neuro-logical examinations; from physical therapy, occupa-tional therapy, and speech-language pathology reports;and from testing described below. RM received physicaltherapy, occupational therapy, and speech therapy fromlicensed therapists for a total of 2 to 3 hours of therapya day, 5 days a week, from 3 days to approximately 41⁄2months post-stroke. Therapy sessions were spacedthroughout the day to minimize fatigue. When improve-ment appeared to reach a plateau, he was dischargedfrom therapy but continued to receive restorative nurs-ing intervention, including training in activities of dailyliving (ADL) and mobility, range of motion (ROM), andsplint management. Generally, RM was cooperative andmotivated during examination and therapy sessions. Heresponded to questions and commands correctly andwithout delay, and he called for assistance when neces-sary. His emotional and social responses were appropri-ate. He became understandably frustrated with hisinability to successfully perform some tasks but exhibitedgood abstract thinking and problem-solving abilities in

devising alternative strategies. For example, he wasresourceful in using environmental support to stabilizehis body or objects he manipulated, and when unable toaccomplish a task one-handed, he used both hands.Physical therapist examination detailed below was per-formed 3 months after his stroke, at Meriter HealthCenter, Madison, Wis.

Posture and Whole-Body MovementsNeuronal damage associated with the hemorrhage in themedial pontine tegmentum resulted in severe deficits ofcontrol of posture, balance, and locomotion. Rollingand transitions from sitting to supine postures werepoorly coordinated, and they were not accompanied bysequential eye, head, or trunk movements and protectiveassistance of the upper extremities. RM was unable to situnsupported, and attempts to use his arms or legs forpostural support were ineffective. He sat with a posteriorpelvic tilt, increased thoracic kyphosis, increased uppercervical extension, and with his head forward. Duringtransitions from sitting to standing, his hips and kneeswere poorly coordinated as evidenced by high variabilityin the temporal sequence of hip and knee extension.Unless he was assisted to keep his hips and kneessomewhat flexed, his center of mass tended to shiftposteriorly and to the left. Videotape review indicatedthat self-induced sway as well as postural adjustments inresponse to externally imposed perturbations wereabsent. Postural alignment and the ability to remainupright while sitting or standing deteriorated furtherwith the eyes closed. When supported upright by aplatform walker that was propelled forward for him, RMwas able to take steps. His base of support was wide. He

* Pfizer Inc, 235 E 42nd St, New York, NY 10017.

Table.Localization of the Hemorrhage in the Medial Pontine Tegmentuma

Sign Implicated Neural Structure Right Left

Vertical movements and adduction of the eyes CN III, IV, oculomotor and trochlear � �

Deviation of the jaw CN V, trigeminal motor � �

Conjugated gaze and horizontal adduction of the eyes CN VI, abducent � �

Facial weakness and difficulties closing the eyes CN VII, facial � �

Balance/equilibrium CN VIII, vestibular components � �

Audition CN VIII, cochlear components � �

Salivatory function CN IX, glossopharyngeal � �

Cheyne-Stokes breathing CN X, vagus � �

Trapezius and levator scapulae muscle function CN XI, spinal accessory � �

Tongue movement and gag reflex CN XII, hypoglossal � �

Contralateral cerebellar signs Central tegmental tract � �

Arousal Nucleus raphe magnus and pontis � �

Discriminative touch/proprioception Medial lemniscus � �

Pain and temperature sensation Anterolateral tract � �

a CN�cranial nerve, minus sign�intact, plus sign�impaired.


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advanced the left leg slowly and stiffly, with lateral(external) rotation and adduction of the hip. Headvanced the right leg using hip and knee flexion. Steplength and height were small and irregular. Although heaccepted weight on the legs with the knees flexed, theknee and hip frequently buckled further into flexion,especially on the right. During stepping, the legsadvanced faster than the trunk, thereby further shiftinghis center of mass posteriorly and to the left.

Independent Limb MovementsDespite severe postural deficits of head, trunk, and limbgirdle, RM made relatively good use of the right handand fingers in isolation, provided the trunk and rightupper arm were appropriately stabilized. For example,with environmental support, he could manipulate smallobjects such as dominoes or simple tools such as atoothbrush. When an object was placed near his righthand in an accessible orientation, he used thumb andforefinger apposition to retrieve and hold on to it. Incontrast, he was unable to grasp an object in his lefthand, and when placed there it easily slipped from hisgrip. He did attempt to use his left arm and hand inconjunction with his right arm and hand for bimanualactivities, such as retrieving or repositioning an object inthe hand, although he used his left limb primarily toassist activities of the right limb. Thus, some functionaluse of the right hand and fingers remained, yet skillfulmanipulation of objects with either hand was poor. RM’svoluntary limb movements were poorly integrated withposture. Videotape review indicated that elevation ofeither arm was not preceded by anticipatory posturaladjustments of the trunk or shoulder girdle and thatpointing or reaching toward visual targets was notaccompanied by sequential eye, head, and arm move-ments. RM pointed without moving his eyes, head, ortrunk. Aiming with both right and left limbs wasaccurate.

Reaching to GraspIn light of the functional specialization of medial versuslateral descending motor systems reviewed in the pre-ceding text, we considered it important to formally testRM’s ability to perform reach-to-grasp tasks. RM and hiswife gave permission to videotape the testing. A beltaround the waist provided support to maintain anupright sitting posture (Figs. 2A and 2D). Prior toreaching, the arm was held loosely at the side, with thepalm down and the forearm pronated. On verbal cue,RM reached to grasp a cylinder (height�15 mm, diam-eter�25 mm) positioned at arm’s length and at shoulderheight, using 1 of 2 types of grasp. One grasp, thewhole-hand grasp, required an overhand scoopingmotion of all 4 fingers to retrieve the cylinder from aclear container (height�50 mm, diameter�100 mm).The other grasp, the precision grasp, required thumb

and forefinger apposition to retrieve the cylinder from ahorizontally oriented slot (width�80 mm, height�30mm). RM’s reach-to-grasp movements were slow andlabored with either arm. Figures 2A through 2F showvideotaped images and stick-figure reconstructions ofthe right arm (Figs. 2A–2C) and left arm (Figs. 2D–2F)during individual trials of performance of the whole-hand task (Figs. 2B and 2E) and precision task (Figs. 2Cand 2F). Records of angles of the metacarpophalangeal,wrist, elbow, and shoulder joints are plotted versus timein Figures 2G through 2J, respectively, for the trialsillustrated in Figures 2B, 2C, 2E, and 2F.

During reaching to grasp with the right arm, RM did notextend the wrist to preshape the hand in preparation forgrasp (Fig. 2H, solid lines), and he did not supinate theright forearm, regardless of task (whole-hand or preci-sion). Therefore, the right hand was not oriented appro-priately relative to the orientation of the target. Despitethe impaired preshaping of the right hand, he was ableto complete a grasp. In contrast, during reaching tograsp with the left arm, the wrist did extend (Fig. 2H,broken lines) and the forearm did supinate to preshapeand orient the hand to the target, regardless of task.Typically, the left hand opened wide but failed to closearound the object grasped.

Localization of the LesionAs neither structural magnetic resonance imaging norpostmortem histology was available, our estimate of thelocation and extent of the neurological damage thatresulted from the hemorrhagic stroke is based on theknown structure-function relationships of brain-stemstructures in combination with correlation of CT scansof the head with matched histological sections. The CTscan shown in Figure 1A was made in the evening of theday of admission when the extent of hemorrhage wasmaximal. An outline of the hyperdense area of the CTscan in Figure 1A is overlaid (broken white line) on amatched histological section in Figure 1C. The plane ofsection (Fig. 1B) is through the sella turcica and thecaudal third of the fourth ventricle, at a 25-degree anglewith respect to the horizontal stereotaxic plane. Thearea of hemorrhage was most extensive medially andcaudally in the pons, including both the right and leftpontine reticular formation. The hemorrhage extendedfarther into the right half than the left half of thepontine tegmentum, with little or no involvement of thebasilar pons.

The extent of the area of hemorrhage agreed well withthe observed clinical signs of damage to cranial nervestructures and motor and somatosensory pathwaysdescribed in the preceding text and summarized in theTable. The oculomotor and trochlear nuclei in themidbrain were not included in the area of hemorrhage,


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Figure 2.Kinematics of the right and left upper extremities during performance of the reach-to-grasp task. (A and D) videotaped images showing the right andleft limbs during performance of the whole-hand task. (B and E, C and F) stick figures of the upper extremity during task performance. Stick figuresof the moving limb were reconstructed and joint angles were calculated from the x-y coordinates of the following landmarks: the head of the humerus,the rotation point of the elbow, the proximal end of the carpals, the proximal phalanges, and the proximal interphalanges. The x-y coordinates forthese points were identified on successive video frames of the moving limb (resolution: 33.3 milliseconds). Each panel illustrates an individual trialof performance of the whole-hand task (panels B and E) and the precision task (panels C and F). Individual lines connect the shoulder, elbow, wrist,metacarpophalangeal, and proximal interphalangeal joints and the tip of the index finger. (G–J) Individual trial records of approximate angles ofmetacarpophalangeal (MCP), wrist, elbow, and shoulder joints are plotted versus time for the trials illustrated in panels B and E and panels C and F. Time0 corresponds to reach onset. The time at which RM contacted the container (whole-hand task) or slot (precision task) corresponds to reach offset.


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which is consistent with retention of vertical eye move-ments. The abducent nuclei, the medial longitudinalfasciculi, and the abducent nerve roots, were included inthe area of hemorrhage bilaterally, which is consistentwith the observed abnormalities in horizontal eye move-ments and conjugated gaze. The genu of the facial nervewere included in the area of hemorrhage bilaterally,which accounts for the observed facial weakness anddifficulties wrinkling the forehead and closing the eye-lids. Components of the medial system of brain-stemdescending motor pathways passed through or wereincluded in the area of hemorrhage bilaterally, which isconsistent with the observed deficits in posture andwhole-limb movements. The entire medial lemniscusand parts of the spinal lemniscus were included in thearea of hemorrhage on the right, whereas only a dorso-medial portion of the medial lemniscus was included onthe left, which is consistent with the observed deficits insomatosensory responsiveness. The raphe nuclei wereincluded in the area of hemorrhage bilaterally, which isconsistent with the observed fluctuations in level ofarousal. The right central tegmental tract was includedin the area of hemorrhage, which is consistent with theobserved rubral tremor. The central tegmental tractconnects the red nucleus with the ipsilateral inferiorolivary nucleus which, in turn, projects to the contralat-eral cerebellum.70,71

Tests and MeasuresExamination results (detailed below) were based onobservations of the first author. Although validity andreliability of measurements were not established for-mally for the purpose of this case report, independenttesting and retesting by individual members of RM’srehabilitation team over the 6-month period after thestroke yielded consistent results.

Mobility. RM’s mobility was quantified by the MinimumData Set (MDS) and the Functional Independence Mea-sure (FIM), administered 2 weeks post-stroke and again3 months post-stroke. The MDS is an instrument that wasdeveloped to rate severity of patient disability and out-comes of medical rehabilitation of individual nursinghome residents. Evidence for validity and reliability ofmeasurements obtained with the MDS has been report-ed.72–74 In brief, MDS scores have been validated bycorrelation with various independently obtained mea-surements of basic behavioral and mental health func-tions (eg, Mini-Mental State Examination, Spearmancorrelation coefficient [r]�.45; Alzheimer’s DiseasePatient Registry, r �.50; Dementia Rating Scale for ADL,r �.59).72 The MDS scores met a standard for excellentreliability in key areas of functional status, such ascognition, ADL, continence, and diagnoses (eg, Spearman-Brown intraclass correlation coefficients were .4 orhigher for 89% of items and .6 or higher for 63% of

items).75 RM assisted in but contributed less than 25% ofeffort required to complete mobility tasks tested, whichclassified him as requiring maximal assistance as definedby Keith et al.76 The MDS scores for mobility (eg, theability to move in bed, perform toilet transfers andhygiene while toileting) improved over the 3-monthperiod from requiring maximal assistance of 2 people(3/8) to requiring maximal assistance of 1 person (2/8).

The FIM is another widely used scale that yields valid andreliable measurements of mobility, locomotion, self-care,sphincter management, communication, and social cog-nition.77–80 Its 7-level scale ranges from “total depen-dence” (0) to “complete independence” (7). RM’s bedmobility improved from requiring maximal assistance(2/7) to requiring moderate to maximal assistance(2.5/7). Transfers improved from requiring maximalassistance (2/7) to requiring moderate assistance (3/7).Walking improved from complete dependence (1/7) torequiring moderate to maximal assistance (2.5/7).Grooming, bathing, toileting, and upper- and lower-body dressing improved from requiring maximal assis-tance (1.7/7) to requiring moderate to maximal assis-tance (2.5/7). Although the increase in scores over the3-month interval between tests appears modest, we con-sider the corresponding improvements in mobilityimportant because they facilitated interactions of RMwith his caregivers, thereby reducing the level of frustra-tion RM experienced as a result of his disabilities.

Psychosocial well-being. Both the MDS and FIM incor-porate measures of psychosocial well-being. Scores ofdichotomous items such as restlessness, variability inmental status, insomnia, and depression improved frombeing present to being absent. In addition, the ability tomake himself understood and interact with others; par-ticipation in planned and structured, and self-initiated,activities; and involvement in the social life of the facilityall improved from being absent to being present. RM’simprovements in dysarthria were large. Three days post-stroke, he was 20% intelligible in conversation; following3 months of speech therapy, he was 60% to 70%intelligible, and he used compensatory strategies such asslow, exaggerated articulation and spelling. Speech ther-apy also addressed his dysphasia. Despite extensive ther-apy, however, he continued to experience difficultiesswallowing while feeding on pureed solids and thinliquids. Therefore, he received his nutrition with enteralfeedings through a gastric tube and only under specialcircumstances (“recreational feeding”), and with carefulmonitoring was he allowed to consume thin liquids bymouth.

Cognition. Psychiatric and neurological consultationsdone approximately 1 year prior to RM’s stroke indi-cated that he had mild cognitive impairment due to


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early-onset dementia related to age, alcohol abuse, orischemic accident. Until the morning of his stroke,however, he continued to function well, at home as wellas at his work as a parking lot attendant. Three days afterthe stroke, RM’s comprehension of written and spokenwords was good, he was able to answer complex yes/noquestions with an 85% success rate, and he followed 2-and 3-step commands. Cognitive performance was for-mally tested using the Ross Information ProcessingAssessment (RIPA),81 an instrument used to identify,describe, and quantify cognitive-linguistic deficits ingeriatric populations. Procedures for establishing normsand evidence for reliability and validity of RIPA scoreshave been reported.81 Content validity has been estab-lished through professional review.81 Analysis of internalconsistency reliability yielded alpha coefficients of .88 to.97.81 Concurrent validity and interrater reliability ofRIPA scores have not been evaluated. RIPA scores indi-cated mild impairment in recent memory (20/24),spatial orientation (14/18), and problem solving/abstract reasoning (22/27) and no impairment in tem-poral orientation (30/30). A diagnosis of mild cognitiveimpairment was confirmed 6 weeks after the stroke bythe same physician consulted 1 year earlier. In conclu-sion, no evidence indicated that RM’s brain-stem strokehad altered his prestroke cognitive abilities.

Somatosensory responsiveness. Examination of somato-sensory responsiveness included testing discriminativetouch, pain and temperature sensation, andkinesthesia.82(pp143–148) Discriminative touch and painand temperature sensation were intact in the rightextremities and were decreased in the left extremities.Kinesthesia was intact in the right extremities and absentin the left extremities.

Muscle function. Muscle tone (ie, resistance to passivestretch) was examined by observing trunk and extremityposture, by palpation, and by monitoring resistance toimposed movements of extremity joints.82(pp183–184) Toneappeared to be decreased in muscles of the trunk andextremities. Manual testing of muscle force, performedaccording to the procedures described by Kendall et al,83

showed that RM was able to hold his hip joint in a flexedposition against moderate pressure (4/5) bilaterally. Hewas able to hold his knee joint in a flexed position and inan extended position against maximal pressure (5/5)and his ankle joint in a dorsiflexed position againstminimal pressure (3� to 4 -/5) bilaterally. On the right,RM was able to hold his shoulder joint in a flexedposition and in an abducted position against moderatepressure (4/5). He was able to hold his elbow jointagainst maximal pressure (5/5) and his wrist and fingerjoints against minimal pressure (3� to 4 -/5). On theleft, he was able to hold his shoulder, wrist, and finger

joints against minimal pressure (3� to 4 -/5) and hiselbow joint against moderate pressure (4/5).

Range of motion of extremity joints. Goniometric mea-surements84 indicated that the range of active supina-tion/pronation and flexion/extension of the elbow,wrist, and finger joints of both upper extremities wasnormal, except for wrist extension on the right, whichwas limited to neutral. With trunk and scapular support,isolated active and passive shoulder flexion was limitedto 155 degrees on the right and 145 degrees on the left.Without trunk and scapular support, isolated activeshoulder flexion was 100 degrees on the right and 80degrees on the left. Passive ROM of the joints of all 4extremities was normal, except for right wrist dorsiflex-ion, which was limited to 20 degrees, and the limitationsin ROM of shoulder flexion noted above.

EvaluationEvaluation of the examination results was in keepingwith the task-oriented approach of Shumway-Cook andWoollacott.85 Based on the examination results, wehypothesized that both motor and somatosensoryimpairments contributed to the severe functional limita-tions that RM experienced as a result of hemorrhagicstroke in the medial pontine tegmentum. Postural con-trol was largely ineffective because of the absence ofboth anticipatory and compensatory postural adjust-ments. Major components of the medial system of brain-stem descending motor pathways (eg, the MLF, whichcarry vestibulospinal fibers and descending fibers of theinterstitial nucleus of Cajal; the predorsal bundles, whichcarry tectospinal fibers; the medial pontine reticularformation, which gives rise to reticulospinal fibers) aswell as ascending somatosensory pathways (eg, mediallemniscus and anterolateral tracts) passed through orwere included in the area of hemorrhage. Therefore,RM’s abnormalities in control of posture and whole-body movements most likely reflected combined damageto medial brain-stem and ascending somatosensory sys-tems. Damage to the MLF helps explain the observedhorizontal gaze paralysis (vertical eye movements wereretained), because the MLF contains fibers importantfor coordinating horizontal but not vertical eye move-ments. Some residual control of the right hand andfingers and, to a lesser extent, the left hand and fingersremained, which probably reflected sparing of cortico-spinal tracts. RM was able to grasp and hold on to objectswith the right hand but not with the left hand, providedthe trunk and proximal arm were supported. However,both the right and left hands were largely ineffectivewhen reaching to grasp. The asymmetry in residual useof the right hand versus the left hand may be accountedfor by more extensive damage to medial lemniscus orrubrospinal fibers on the right than on the left.


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Intervention and OutcomesIntervention during the period from 3 days to approxi-mately 41⁄2 months after the stroke was based on theapproach advocated by Shumway-Cook and Woolla-cott.85 They suggested that 4 key elements contribute tocomprehensive clinical practice: (1) The problems andneeds of the patient drive the gathering of informationand the development of the plan of care; (2) recognitionthat disablement is affected by disease at several levels,such as impairment, motor strategy, and functionallimitation, allows the therapist to develop a list of deficitsat each of the levels, toward which intervention can bedirected; (3) the nature and cause of deficient motorcontrol are systematically tested (hypothesis-orientedclinical practice); and (4) assumptions related to thenature and causes of deficient motor control have theirfoundation in a scientifically based theory of motorcontrol.

Because RM’s comprehension, memory, judgment, andproblem-solving abilities were retained after the stroke,the care plan emphasized that he be allowed, andencouraged, to direct his activities and to make as manydecisions for himself as possible. He chose to spend lesstime and energy on self-care activities, such as dressingand personal hygiene, which were energy consumingand not rewarding to him. Instead, he spent more timeand energy on the things he really enjoyed, such asone-on-one social activities with family members. Visitinghis family required training family members in how toassist him with car and chair transfers. Sliding board andsquat pivot transfers were safer and more efficient thanstanding pivot transfers because, when assisted to remainin a flexed position, RM did not lose his balance. RM’swife learned how to help him get in and out of his chairand in and out of the car, so they were able to tempo-rarily leave the nursing facility. RM’s wife was emotion-ally and physically supportive of her husband. She visitedhim daily, attended therapy sessions, and assisted RMwith mobility and daily cares. She appeared andreported being physically and mentally healthy, and sheappeared to handle this difficult situation well. Use of anelectric wheelchair would have provided RM withincreased mobility and a sense of independence andcontrol, but was not implemented because of a prognosisfor short life expectancy and financial considerations.

Adaptive equipment and specific compensatory move-ment strategies were implemented in an attempt to assistRM to regain control of some movements, largelybecause of his undiminished cognitive abilities after thestroke. He and his caregivers were trained to support histrunk and proximal limb joints to allow use of the righthand in playing games, such as dominoes, or to assist inself-care activities that he chose to do. During the day,RM wore a lightweight cock-up hand splint that posi-

tioned his wrist in 20 degrees of dorsiflexion. The splintwas designed to improve wrist alignment and stability topromote use of the hand and fingers. (Grasping andmanipulating objects with the wrist flexed is difficultbecause of passive insufficiency of finger flexor muscles.)We taught RM simple strategies, such as resting his armon a support surface and placing his work close to hisbody, to further improve hand use. Stabilization of jointsproximal to the hand is important to manual dexterity ingeneral86; however, our observations suggest that provid-ing stabilization is essential following stroke in themedial pontine tegmentum of the brain stem.

The specific problems RM experienced were not limitedto motor deficits but extended to difficulties in interper-sonal communication and a sense of diminished controlover his life. RM’s appearance (resulting from damage tocranial nerves), low level of arousal, difficulty speaking,and extreme dependence in mobility (detailed in thepreceding text) led people to believe—erroneously—that he had aphasia and cognitive impairment. It seemedimportant for his quality of life that those working withhim realized that he comprehended what had happenedto him and that he was devastated by the inability tocontrol movements of his body. Motor rehabilitation, tosome extent, also served to fulfill RM’s social andemotional needs and his desire for purposeful activity inhis life. For example, when RM was assisted in forwardpropulsion by a platform walker, he was able to bearweight on his legs and activate large muscle groups.Thus, gross motor physical activity (“walking for exer-cise”) was incorporated into the care plan both forgeneral exercise and to attempt to promote positivefeelings of well being, accomplishment, and self-esteem.Such “quality-of-life experiences” may influence posi-tively the mental and physical health of people who arestruggling with loss of functioning and diminished con-trol over their lives.87,88

In summary, during the 41⁄2-month period after thestroke, RM regained his ability to effectively communi-cate his needs and wishes, thereby restoring control overmany aspects of his daily life. Mobility and ability toperform self-care activities improved to the point that herequired assistance of 1 person rather than 2 people.With environmental support and the use of a wrist splint,he regained some hand use. Up to the time of his death,he continued to participate in a restorative program ofexercise and ambulation designed to promote physicaland mental well-being.

DiscussionRM’s deficits in control of posture and whole-bodymovements are consistent with functional contributionsof medial brain-stem descending motor pathways asrevealed by studies of postural control in humans and by


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animal experiments. Studies of automatic posturalresponses to mechanical perturbations in control sub-jects and in people with postural deficits have providedinsights into the neural control of postural stability,89–92

and they have implications for physical therapy prac-tice.93 Current understanding of the neural substratesthat underlie control and integration of posture andvoluntary movements, however, remains fragmentaryand depends largely on results of animal experiments.

RM’s severe deficits in control of posture and whole-body movements and less severe deficits in control ofhand and finger movements were similar to but moresevere than those observed in monkeys with lesions ofmedial-system pathways.5 Thus, our observations indi-cate that the contributions of the medial brain-stem andcorticospinal systems to motor control are functionallydistinct in humans, as they are in monkeys. In monkeys,the corticospinal system does compensate to someextent for loss of function of the medial brain-stemsystem because motor deficits following lesions of themedial brain-stem system were less severe in animals thathad not undergone a bilateral pyramidotomy before thelesion as compared with animals that had fully recoveredfrom prior bilateral pyramidotomy.5 The severity of theobserved deficits in RM’s posture and whole-body move-ments and their persistence for the entire 6-monthsurvival period, in combination with the observation thatthe corticospinal system was largely spared, suggest thatthe corticospinal system provides little or no compensa-tion for loss of function following damage to the medialbrain-stem system in humans.

One caveat is that RM’s fluctuating level of alertness mayhave slowed or impeded developing compensatorymovement strategies. Invoking corticospinal pathwaysmay require adequate motivation and attention, whichRM may only have had periodically due to damage to theraphe nuclei and the locus coeruleus, which give rise toextremely widespread ascending and descending projec-tions that terminate in structures throughout the centralnervous system. These projections mediate diffuse influ-ences on a number of behavioral, physiological, andneuroendocrine functions that are important for regu-lating arousal, sensory awareness, motor responsiveness,and the level of consciousness (for reviews, see Brodal94

and Saper95). Pharmacological intervention, using drugsthat modulate the level of specific neurotransmitters,such as noradrenaline (neurotransmitter in the locuscoeruleus) and serotonin (neurotransmitter in theraphe nuclei), combined with physical therapy has beenreported to enhance motor performance followingstroke.96–102 Use of drugs such as amphetamine assumesthat sufficient numbers of noradrenergic projections areretained to facilitate neurotransmitter release. Pharma-cological intervention might have improved RM’s atten-

tion and ability to utilize sensory information but was notimplemented.

The asymmetry in RM’s residual control of the righthand versus the left hand may reflect different func-tional contributions of rubrospinal versus corticospinaltracts to the control of hand use similar to thoseobserved in monkeys.5 Alternatively, or in addition, RM’snonfunctional grasp of the left hand may have resultedfrom more extensive damage to the right than leftmedial lemniscus at the level of the pons, as use of handand fingers is severely compromised by loss of proprio-ception.103 RM’s preserved ability to produce a func-tional grasp with the right hand in isolation may havereflected sparing of corticospinal tracts. RM’s deficit inextending the right wrist and fingers to preshape thehand during reaching to grasp may have resulted largelyfrom damage to the right rubrospinal tract. The viewthat rubrospinal neurons are important for controllinghand preshaping during reaching to grasp is consistentwith recent results of single-unit recording studies innonhuman primates.25

Although the rubrospinal system is important for handuse in nonhuman primates,25,26 little is known about thecontribution of rubrospinal fibers to control of move-ments in humans. Rubrospinal contributions are com-monly considered less important in humans than inmonkeys because the number of large red nucleus cellsis much smaller in humans104 and, correspondingly,fewer large-diameter rubrospinal fibers have beenobserved in humans than in monkeys.71 In addition,human rubrospinal fibers could not always be tracedinto the spinal cord, and in cases in which a spinalprojection was recognized, few rubrospinal fibers wereobserved below C3.71 If one assumes that rubrospinalfibers originate primarily from large red nucleus neu-rons, the above histological studies support the view thatthe rubrospinal tract may be rudimentary in humans.71

However, the size of the rubrospinal tract in humansmay be underestimated if a substantial number of rubro-spinal neurons are small.105 There is some support forthis view as there is evidence that rubrospinal fibersoriginate from small cells in humans,70,106 mon-keys,107–110 and cats.111 Furthermore, observations of fewrubrospinal fibers below C371 are consistent with theview that rubrospinal neurons in humans may exert theirinfluence on limb movements indirectly, via projectionsto propriospinal neurons in upper cervical segmentsrostral to C3. This view derives support from histologicalobservations in humans that propriospinal neurons inupper cervical segments project extensively into thecervical enlargement.112 Thus, the conclusion that thehuman rubrospinal tract is rudimentary may be prema-ture—damage to rubrospinal pathways may have con-tributed to the observed deficits in RM’s hand use.


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ConclusionTherapeutic intervention aimed at optimizing residualcontrol of the distal extremities appears beneficial forrehabilitation of people with either cortical or brain-stem stroke. This case suggests, however, that peoplewith a stroke affecting the medial brain-stem systemneed to be provided with support of the trunk andproximal limb during activities. Positive social interac-tions and a sense of well-being, accomplishment, andself-esteem appear to be equally important. This casesuggests that the latter are especially important followingbrain-stem stroke because the patients’ appearance andfluctuating level of arousal may obscure their undimin-ished cognitive and emotional functions. We believe thatphysical therapist examination and recognizing intactmotor and cognitive functions following brain-stemstroke can aid in developing intervention strategies thatmaximize rehabilitation and quality of life.

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