546

Cerebral Diaschisis Following Cerebellar Hemorrhage
Harris S. Hausen, MD, Elisabeth A. Lachmann, MD, Willibald Nagler, MD
ABSTRACT. Hausen HS, Lachmann EA, Nagler W. Cerebral diaschisis following cerebellar hemorrhage. Arch Phys Med
Rehabil 1997;78:546-9.
In 1914, Von Monakow described diaschisis, the recovery of
lost cortical function in regions positionally distant from, but
linked by neuronal tracts to, the primary site of cortical damage.
Cerebellar diaschisis after cortical insult is detailed in the literature; however, cortical diaschisis after cerebellar insult remains
a rarely reported occurrence. We describe a 36-year-old woman
with rupture of a right-sided cerebellar arteriovenous malformation who developed such expected cerebellar signs as ataxia,
dysmetria, and nystagmus. Days later, the patient developed
profound impulsivity, disinhibition, and psychomotor agitation.
Single photon emission computed tomography (SPECT)
showed decreased perfusion of the bilateral frontal and temporal
lobes, consistent with regional loss of neural activity. Eventual
clinical improvement corresponded with reperfusion of those
regions, identified on follow-up SPECT. This case documents
cortical diaschisis following cerebellar insult and shows that
diaschisis must be considered in patients with cerebral injury
manifesting cortical deficits remote from the site of primary
pathology.

© 1997 by the American Congress of Rehabilitation Medicine
and the American Academy of Physical Medicine and Rehabilitation
S EARLY AS 1914, Von Monakow I described diaschisis
from the Greek meaning "throughout," and
"-schisis," from the Greek meaning "split,"), 2'3 a controversial
theory characterized by "the abolition of [neuronal] excitability" and " a functional standstill" of neuronal activity within
the brain. Diaschisis was seen as the cerebral counterpart to
spinal shock in which, akin to the temporary decrements or
abolition of spinal reflexes distal to the level of spinal cord
transection, cerebral injury in one locale caused decrement of
function in a distant region of the brain via interruption of
linking neuronal tracts. 4 Three subtypes of diaschisis are detailed: (1) diaschisis cortico-spinalis, in which trauma of the
motor cortex produces a loss of function within the spinal cord,
progressing along fibers of the pyramidal tracts; (2) diaschisis
commisuralis, in which trauma of the cerebral cortex of one
hemisphere results in loss of function in a contralateral region
of the brain, progressing along the linking axons of the corpus
callosum; and (3) diaschisis associativa, in which trauma of one
cortical area results in loss of function in nearby, or neighboring,
intact cortical areas, progressing along intracortical fibers.
Much of Von Monakow's theory expanded on earlier works

A ("dia-,"

From the Department of Rehabilitation Medicine, The New York HospitalCornell Medical Center, New York, NY.
Submitted for publication April 29, 1996. Accepted in revised form September
17, 1996.
No commercial party having a direct or indirect interest in the subject matter
of this article has or will confer a benefit upon the authors or upon any organization
with which the authors are associated.
Reprint requests to Harris S. Hausen, MD, Department of Rehabilitation Medicine, The New York Hospital-Cornell Medical Center, 525 East 68th Street, F18, New York, NY 10021.
© 1997 by the American Congress of Rehabilitation Medicine and the American
Academy of Physical Medicine and Rehabilitation
0003-9993/97/7805-4001$3.00/0

Arch Phys Med Rehabil Vol 78, May 1997

of Brown-Sequard, 5 who proposed that injury in one cortical
locus may cause a loss of excitatory, or negatively excitatory
(ie, inhibitory) input to other, possibly distant, loci. It is the
abolition of this excitatory input from the injured cortical region
through the presumed connecting neuronal tracts to areas positionally adjacent or afar that typifies diaschisis. The trauma to
the injured region usually appears suddenly, as in the case of a
cerebrovascular accident (CVA), but it may rarely present as a
"slowly creeping diaschisis"6 resulting from, for example, the
mass effect of a slowly growing tumor; the damage progresses
in a wavelike manner, propagating along the neuroanatomic
pathways from the site of primary trauma. Modem use of computed tomography (CT), magnetic resonance imaging (MRI),
and single photon emission computed tomography (SPECT)
allow precise localization of cerebral injury after infarct or hemorrhage.
We describe a patient who developed a right-sided cerebellar
hemorrhage with subsequent loss of function, and later restoration of function, of the bilateral frontal and temporal lobes.
Whereas cerebellar diaschisis following primary cortical insult
has been sufficiently discussed in the literature, the paucity of
relevant material documenting primary cerebellar damage with
resultant cortical symptomatology substantiates the findings of
Botez 7 and Rousseaux s that such cerebello-cortical diaschisis
is indeed a very rare occurrence. The rehabilitation professional,
however, should be aware of the existence of diaschisis and the
role, and limitations, of a well-directed program of physiatric
intervention.
CASE DESCRIPTION

A 36-year-old right-handed nurse developed the sudden onset
of dizziness and loss of balance while working in the intensive
care unit. She excused herself from work, believing that she
had a mild viral infection; however, the dizziness progressed
over the ensuing few hours such that she was unable to stand,
falling to the right side. She also developed nausea, vomiting,
mild chills, and a right-sided headache. The patient denied dyspnea, cough, pharyngitis, visual disturbances, or cognitive impairments. Her medical history was notable for a mild, bilateral
sensorineural hearing loss, with slightly poorer threshold of the
right ear, diagnosed 5 years prior to the present event. She
specifically denied a history of similar episodes of dizziness,
recent head trauma, fever, diabetes, hypertension, known neoplastic disease, or human immunodeficiency virus (HIV) risk
factors. She had no known allergies or prescriptions for medications. The patient smoked one pack of cigarettes daily, having
a 15 pack-year smoking history, and consumed one or two
alcoholic beverages weekly. She denied the use of oral contraceptives or narcotics.
On examination, the patient's vital signs were stable and she
was found to be alert, oriented to person, place, and time, and
cooperative with the examiners. There was no apparent cranial
trauma. Although her extraocular muscles were grossly intact
and the fundoscopic exam was unremarkable, she did display
a lateral-gaze paretic nystagmus of both eyes, the right more
severely affected than the left, requiring repetitive saccades to
gaze rightward. Her pupils were round and reactive to light. On
gross examination her hearing was diminished bilaterally, the
right side more greatly affected than the left; however, both

CEREBELLAR-CORTICAL DIASCHISIS, Hausen

Fig 1. Axial MRI showing right-sided cerebellar hemorrhage.

Rinne and Weber hearing tests were within normal limits. Motor
strength was found to be 5-/5 throughout all extremities; however, the patient had substantial right-sided dysmetria, particularly evidenced by poor performances of finger-to-nose and
rapid-alternating-movements (quick and successive alternation
of hand pronation/supination positioning and foot-tapping) of
the right upper and lower extremities, respectively. Fine motor
skills of the right hand were substantially impaired. Her gait
was wide-based with a rightward list. Deep tendon reflexes were
normal throughout all extremities and the patient had a normal
gag reflex without apparent difficulty swallowing, but she did
have mildly dysarthric speech. Sensory examination to light
touch and pinprick were normal, as was evaluation of the cranial
nerves. Hemogram, serum electrolyte, and glucose values were
unremarkable. The remainder of the physical examination was
unremarkable.
MRI of the brain showed a large hematoma in the right
cerebellar hemisphere with moderate mass effect of the soft
tissue (fig 1). CT showed no other sites of cerebral infarct or
hemorrhage. Angiography of the right vertebral artery and right
external carotid artery demonstrated normal vascular anatomy
of the major cerebellar branches; however, an identified area of
contrast blush lasting through the capillary phase, into the venous phase, was consistent with arterio-venous malformation
(AVM) rupture. Audiometric studies revealed mild-moderate
sensorineural hearing loss with poorer thresholds of the right
ear, essentially without change since diagnostic workup 5 years
earlier.
Admitted to the neurology service with a diagnosis of ruptured right-sided AVM, the patient was initially managed with
supportive care and intravenous steroid therapy, (dexamethasone, 6mg four times daily) for 48 hours to minimize the cerebellar mass effect and edema; she was subsequently transferred

547

to the rehabilitation medicine service for continuation of her
care. Over the following few days, she became increasingly
lethargic with worsening difficulties in concentration and cognition. She reported no improvement in the dizziness, and the
ataxic gait and rightward list remained unimproved. The patient
progressed to develop impulsive and unsafe behavior, frequently attempting to climb over the bedrails or ambulate without assistance, despite multiple falls. Her actions necessitated
engagement of a full-time attendant to ensure her safety. She
displayed progressively diminished inhibitions, presenting in
public areas partially disrobed, violently refusing bathing or the
changing of soiled clothing, and directing verbal and physical
outbreaks at the medical and nursing staff. She nevertheless
remained globally oriented and reported being aware of her
behavior but unable to control it; she stated a perpetual feeling
of anxiety and was noted by the staff to display substantial
psychomotor agitation while in bed or sitting in a chair. Accordingly, she was unable to participate in physical therapy and
occupational therapy sessions.
The patient's vital signs and laboratory values, including
hemogram, biochemical profile, thyroid function studies, Lyme
titer, and erythrocyte sedimentation rate, were within normal
limits. Neurobehavioral evaluation found mild-moderate deficits
in concentration, moderate difficulties with abstractional abilities, severely diminished verbal fluency, and severe motor perseveration, bilaterally, on 3-step sequential hand movements;
these findings were suggestive of frontal lobe dysfunction.
SPECT evaluation showed decreased perfusion of the central
area of the right cerebellum, as was expected. SPECT additionally revealed dramatically reduced perfusion of the bilateral
frontal and temporal lobes, consistent with the decrement, or
loss, of neural activity in these regions (fig 2).
The patient was placed on a program of physical therapy and
occupational therapy, although progress was initially limited as
a result of her profound mental status changes. Over the following 3 months, the patient's impulsive behavior, psychomotor
agitation, and cognitive functioning gradually improved,
thereby enabling her participation with physical therapy and
occupational therapy sessions. Repeat SPECT evaluation, approximately 16 weeks after rupture of the AVM, showed further
decreases of perfusion in the area of damage of the right cerebellum, representative of neural demise in that area. However,
improvements in perfusion of the bilateral frontal and temporal
lobes were noted, left side somewhat greater than right side,
indicative of neurologic and functional recovery in those areas.
On latest follow-up examination, approximately 13 months
after AVM rupture, the patient continues to have occasional
dizziness and, thus, does not yet drive. Her progress with rehabilitative therapy, however, has allowed for her safe return to
work as a nurse and resumption of most of her other usual daily
activities.
DISCUSSION
Most authors believe that diaschisis is best described as a
theory of functional recovery 5'9-1~ that may be accomplished
through varied mechanisms. Redundancy, or the assumption of
function by uninjured, and previously underutilized, neurons
within the damaged area, and vicariation, or the assumption by
other cortical areas of function that was formerly ascribed to
the now-damaged area, may gradually effect resolution of the
injury. The acquisition of alternate behavioral strategies and
mechanisms, or behavioral substitution, to compensate for the
deficit may also be instrumental in the ensuing recovery of
function. Feeney4 emphasizes that reversibility of the damage
is requisite in the definition of diaschisis, because it is this
aspect that distinguishes diaschisis from the effects of direct
Arch Phys Med Rehabi! Vol 78, May 1997

548

CEREBELLAR-CORTICAL DIASCHISIS, Hausen

Fig 2. (A) Sagittal and (B) transaxial SPECT images shortly after rupture
of right-sided AVM (rows I and 3), and corresponding sections on followup SPECT 16 weeks later (rows 2 and 4). Note improvement in bilateral
frontal and temporal lobe perfusion on later exam.

primary injury. Thus, recovery of function is paramount in the
diagnosis of diaschisis.
Regions of thalamic hypoperfusion, associated with hypometabolism, have been studied with SPECT evaluation in patients
with recent isehemic or hemorrhagic CVA. 12-~7 Recovery in
cortical metabolism, as evidenced by improvement in perfusion
on serial SPECT evaluation, corresponds with clinical improvement. In 1980, Baron 18'a9 using positron emission tomography
(PET) evaluation, described hypometabolism of the cerebellar
hemisphere contralateral to supratentorial infarct. As many as
50% of patients with hemispheric stroke may manifest contralateral cerebellar hypoperfusion, as evidenced on SPECT imaging.ZO22 Contralateral cerebellar hypometabolism after injury
of the frontal cortex, specifically, has also been observed. 16'z3'24
The size and locale of the primary cortical lesion are considered

Arch Phys Med Rehabi| Vol 78, May 1997

the best predictors of contralateral cerebellar hypometabolism
in patients who have suffered a CVA; the density of the resultant
hemiplegia is a much less reliable predictor of distant hypometabolism. 4 Likely, an interruption of the cerebro-cerebellar loop
causes this phenomenon of "crossed cerebellar diaschisis ''8'18
yielding distant metabolic, hence functional, loss. 19'25
It is much more rare to observe hypoperfusion of the contralateral cerebral hemisphere after a unilateral cerebellar injury. 7'8'26Proposed mechanisms include retrograde degeneration
of the fibers of the cortico-pontine tract and the ablation of
excitatory fibers originating within the cerebellum and terminating within the frontal lobes. 7'8'27-29 Frontal lobe injury would
readily explain our patient's poor performance of concentration
skills, abstractional abilities, verbal fluency, and regulation of
motor behavior; temporal lobe injury may further explain our
patient's dramatic emotional and behavioral changes. 3° The patient clearly had damage of the right cerebellar hemisphere as
evidenced by the findings of MRI and angiography as well as
by the severe dizziness, nystagmus, and ataxia found on clinical
examination. SPECT evaluation, revealing hypoperfusion of the
right cerebellar hemisphere as well as of the bilateral frontal
and temporal lobes, confirmed the presence of discrete cerebellar injury with distant cortical dysfunction. Repeat SPECT evaluation, 16 weeks later, paralleled the patient's clinical improvemerit, showing improved perfusion, ie, functional recovery,
within the bilateral frontal and temporal lobes. Whether this
functional recovery had occurred via the mechanisms of redundancy, vicariation, behavioral substitution, or other, presently
unidentified means is of somewhat lesser concern than the fact
that recovery had occurred. The neurons of the right cerebellar
hemisphere were found, on the repeat SPECT evaluation, to
have undergone irreversible injury, or death, whereas neurons
of the bilateral frontal and temporal lobes were seen to return
function to those regions. These findings correspond well with
the observed improvements in the patient's mental and behavioral status. As her concentration, attention span, and emotional
regulation improved, allo,wing her active participation with the
prescribed rehabilitative therapies, the patient was able to learn
compensatory techniques for the cerebellar deficits, ultimately
enabling her return to work and other usual activities.
Included within our differential diagnosis was frontal lobe
degeneration, of multiple etiologies; however, the patient's frontal lobe symptomatolgy resolved after a few months without
intervention. Further, SPECT evaluations revealing initial hypoperfusion, and subsequent reperfusion, of the bilateral frontal
and temporal lobes closely paralleled her clinical status. Because her vital signs and laboratory values were within normal
limits, the patient's presentation of behavioral change was not
consistent with an abnormal metabolic condition and resultant
anoxic/ischemic encephalopathy, hypercapnic encephalopathy,
hypoglycemic encephalopathy, hepatic encephalopathy, or uremic encephalopathy. Also, the patient's afebrile state, absence
of an elevated leukocyte count, and lack of disturbance in such
indicators of homeostasis as heart rate, respiratory rate, and
blood pressure bespeaks a nonseptic process. That a depressive
episode could account, solely, for the patient's mental status
changes ignores the impairments in verbal fluency, abstractional
skills, regulation of motor behavior, and profound impulsive
behavior exhibited, Given that intravenous steroid therapy was
administered for only 48 hours, and that the frontal lobe symptoms did not become manifest until days after discontinuation of
the dexamethasone, in the absence of other known psychotropic
medications it is unlikely that the mental status changes were
induced by steroids or other pharmacotherapeutics. 31 Further,
that the frontal lobe symptoms did not manifest until days after

CEREBELLAR-CORTICAL DIASCH|SIS, Hausen

the A V M rupture is consistent with the model of a propagated
w a v e of damage.
Thus, recovery of diminished function in an otherwise intact
region of the brain, remote from that of the primary injury but
secondarily affected via disruption of cross-linking neuronal
tracts, is the hallmark of diaschisis. Typically, diaschisis occurs
in a cortical-cerebellar direction. Rarely, as in the case we present, does diaschisis manifest in a cerebellar-cortical fashion.
Although it is a rare entity, cerebellar-cortical diaschisis must
be considered when evaluating patients who manifest symptoms
of cortical hemispheric injury apparently remote from the site
of primary cerebellar insult. Academically, this case provides
further evidence of the presumed, well-developed functional
interconnections between the cerebellum and the cerebrum in
humans. 32 The tenets of diaschisis also may explain the behavioral changes often seen in patients who have survived a CVA.
These behavioral and mental status changes may greatly affect
the patient's ability to partake in, and benefit from, rehabilitation
therapy. Recommendations for therapy may need to be postponed until the patient's cognitive level allows for the learning
of safe and efficient strategies of compensation and restoration
of function. Finally, an awareness of these issues allows physicians and therapists to be better equipped in diagnosing and
managing patients with such processes, yielding more properly
directed and effective care.
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