58

Surg Neuroi
1993 ;39:58-65

Spontaneous Midbrain Hemorrhage : Report of Seven New Cases
Michael J . Link, M.D., J. D. Bartleson, M .D., Glenn Forbes, M.D .,
and Fredric B . Meyer, M .D.
Deparrments of Neurosurgery, Neurology, and Diagnostic Radiology, Mayo Clinic and Mayo Foundation,
Rochester, Minnesota

Link MJ, Bartleson JD, Forbes G, Meyer FB . Spontaneous

midbrain hemorrhage : report of seven new cases . Surg Neurol
1993 :39:58-65 .

Spontaneous midbrain hemorrhage is a unique brain-stem
vascular lesion . Sixty-six cases have been reported in the
literature, to which we add seven .
Of the total of 73 patients reviewed, most presented
acutely (66%), but subacute (22%) and chronic onsets
(12%) also occurred . Neuro-ophthalmologic abnormalities were found in 88% of patients. Some alteration of
consciousness and headache occurred in most patients .
Hemiparesis, hemisensory loss, and ataxia were less frequent manifestations .
Vascular malformations were suspected or proved in
37% of patients, hypertension was present in 219, and a
bleeding diathesis was noted in 5% . No underlying cause
was apparent in 37% .
Most patients improved with supportive care only . At
follow-up, 235E of patients had no neurologic deficits . In
51% of patients, minor neurologic deficits persisted, related chiefly to cranial nerves III and IV. Moderate deficits
persisted in 16% of patients, and 5% of patients died .
KEY WORDS: Midbrain ; Hemorrhage ; Arteriovenous malfor-

mation ; Upgaze paresis

Primary midbrain hemorrhage is a rare clinical event. An
extensive search of the literature through 1990 for cases
of spontaneous, isolated, nontraumatic midbrain hemorrhage revealed 48 publications reporting 66 such patients
{1,2,4-10,12-16,18,20-25,27-30,36-39,41,
43-49,51-58,60,62,63] . The Mayo Clinic experience
has been seven patients with spontaneous midbrain hemorrhage (SMH) between 1976 and 1990. The cases from
the literature and those from the Mayo Clinic records
were reviewed to help determine the incidence, etiology, clinical presentation, methods of diagnosis, possible
treatment options, and prognosis for SMH .
Address reprint tegae t, tc J . D. Bartleson, \r . D.., Mayo Clinic, 200
First Street SW, Rochester, Minnesota 55905 .
Received April 20, 1992 : accepted May 13, 1992 .

0 1993 by Flsetiier Science PubUshin5 Co ., Inc .

Methods
The medical records of all Mayo Clinic patients with the
diagnosis of intracraniai hemorrhage between January 1,
1976, and December 31, 1990 were reviewed (i .e ., since
the widespread availability of computed tomography) .
Included were patients who had a spontaneous, nontraumaric, intra-axial hemorrhage that affected and was
largely confined to the midbrain . Cases were not excluded if obstructive hydrocephalus or moderate intraventricular hemorrhage was present . Computed tomographic (CT) and magnetic resonance imaging (MRI)
scans were reviewed by one of the authors (G.F .) to
verify the location of the bleeding .

Results
Seven Newly Described Patients
Case 1 . A 75-year-old man was found unconscious
with a fixed, dilated right pupil. He had a history of
hypertension and was taking warfarin because of a history of transient ischemic attacks . His prothrombin time
was prolonged (57 s ; control 10 .9-12 .8 s). A CT scan
showed a large hemorrhage affecting the entire midbrain
with some blood in the third ventricle and obstructive
hydrocephalus . His condition deteriorated, and he died
36 hours after onset .
Case 2 . A 5 5-year-old man presented with a 3-month
history of progressive left limb weakness with at least
one episode of sudden worsening . There was a history
of hypertension . A CT scan showed a 1-cm hemorrhage
in the right cerebral peduncie . An angiogram was normal- His deficit stabilized .

Case 3 . A 51-year-old woman noted the sudden onset
of dysequilibrium followed by right-sided numbness,
drowsiness, blurred vision, bilateral tinnitus, and some
headache . On examination, she was drowsy, with bilateral ptosis and speech and gait ataxia. There was a history
of migraine . CT and MRI scans showed a 1-cm hemorrhage in the left midbrain tectum, with mild hydrocepha0090-i 019.. 93.. SI3 .00

Spontaneous Midbrain Hemorrhage

Figure 1 . Case 4 . (Left) Unenhanced CT scan on day of hemorrhage,
showing hyperdense zone representing hemorrhage in right side of midbrain
rectum . (Right) MRI scan 6 days later, showing hyperintense signal on
short-TElshort-TR sequence within the inferior colliculus, consistent with
a subacute or chronic component of hemorrhage .

lus . An angiogram showed an arteriovenous malformation in the collicular plate . She underwent surgical
exploration elsewhere, but the malformation was unresectable . She then underwent gamma knife irradiation .
One year later, persistent diplopia developed . Three
years after her bleed she had mild memory loss, bilateral
ptosis, nystagmus, paresis of both medial recti and left
superior rectus muscles, and moderate speech and mild
gait ataxia .
Case 4 . A 44-year-old women noted the sudden onset
of headache, dizziness, bilateral tinnitus, and transient
drowsiness . On examination, she was noted to have mild
left lower facial weakness, mild left hemihypalgesia, and
a subtle left fourth nerve paresis . CT and MRI scans
showed a 0 .5-cm hemorrhage in the right midbrain tectum (Figure 1) . An angiogram was normal . Her signs and
symptoms completely resolved within 3 months .
Case 5 . A 71-year-old man noted the sudden onset
of transient unconsciousness followed by headache and

Surg Neural
1993 ;39 :58-65

59

confusion (which cleared), left limb numbness, and diplopia . Examination showed mild gait ataxia and a left
fourth nerve paresis . He had been taking 5 grains of
aspirin a day . A CT scan showed a 0 .5-cm hemorrhage
in the right midbrain tectum . An angiogram was normal .
A subtle left fourth nerve paresis persisted .
Case 6 . Lethargy, bilateral ptosis, and left hemiparesis
developed in an 87-year-old man over 24 hours on the
day after a left axillary artery thrombectomy and heparinization . Examination showed stupor, Cheyne-Stokes respirations, bilateral third nerve paresis (greater on the
right side), and left hemiparesis . There was a history of
diabetes mellitus, chronic atrial fibrillation, and remote
stroke . A CT scan showed a 1 .25-cm hemorrhage in the
right cerebral peduncle (Figure 2) . He was improving
neurologically when he died in a nursing home of medical complications 4 weeks after the hemorrhage .
Case 7 . Ataxia, headache, and lethargy developed in
a 30-year-old woman during her seventh month of pregnancy . During her ninth month, these symptoms increased and diplopia developed . After cesarean section,
her condition worsened again . Examination showed stupor, bilateral third nerve paresis (greater on the left
side), and diffuse hyperreflexia . At age 14 years, she had
had a right hemiparesis, ataxia, and diplopia and was

60

Surg Neurol
1993 ;39 : 5 8-65

Link et al

tensive intraparenchymal hemorrhage (17] . Dinsdale
[11] also noted no midbrain lesions among 510 intracerebral hemorrhages in 19,000 autopsies over 20 years,
predominantly in a hypertensive population . Roig et al
[431 reported that of 277 patients in whom the diagnosis
of intracerebral hemorrhage was made by clinical examination and CT, three had localized midbrain hemorrhages . Mangiardi and Epstein [34] collected from the
literature 51 cases of brain-stem hematomas that underwent neurosurgical intervention and found that the site
was in the midbrain in five .
The medical records of approximately 1750 patients
with the diagnosis of intracranial hemorrhage seen at the
Mayo Clinic were reviewed, and seven with SMH as
defined above were discovered . Patients with a history
of trauma or a primary infarction with secondary hemorrhage were excluded . Not all patients with the diagnosis
of intracranial hemorrhage underwent an appropriate
imaging procedure or autopsy examination . Thus, we
estimate that the frequency of SMH is between 0 .5%
and 1.0% of all spontaneous, primary intracranial hemorrhages seen at our institution .
Etiology

Figure 2 . Case 2 . Unenhanced CT scan, showing 1 .25-cm hyperdense
zone representing hemorrhage in right cerebral peduntle.

found to have an enlarged brain stem . She was treated
with a shunt and irradiation at that time . CT and MRI
scans obtained during her current episode showed multiple angiographically occult vascular malformations with
a 3-cm hemorrhage in the central midbrain . A cerebral
angiogram was negative . She slowly and incompletely
improved .
Literature Cases

The 66 cases in the literature are summarized and compared to our seven patients in Tables I through 6 .
Discussion
Incidence
The true incidence of isolated SMH is difficult to determine . The frequency of SMH has been variously related
to the number of intracerebral hemorrhages, posterior
fossa hemorrhages, and brain-stem hemorrhages . Thus,
comparison of reports is difficult, if not impossible . The
majority of brain-stem hemorrhages, especially those
associated with hypertension, are pontine . There were
no cases of midbrain hemorrhage in Freytag's anatomopathologic series of 393 patients who died from hyper-

A clear cause for SMH can be difficult to identify . Hemorrhage secondary to a vascular malformation (VM) is
the most frequently cited cause . Such malformations
include arteriovenous malformations (AVMs), cavernous malformations, venous malformations, and telangiectasias . AVMs are visible on angiography ; venous malformations can be seen in the venous phase only .
Cavernous malformations and telangiectasias are not
usually seen on angiography [501 . Cryptic or thrombosed malformations may be detected with either CT or
MRI, and indeed, a higher level of detection of such
incidental lesions can now be expected, with the more
widespread use of MRI .
Of the cases reported in the literature, 10 patients
(15%) had small midbrain VMs detected at operation,
by angiography, or at autopsy. Fifteen patients (23%)
were suspected to have VMs by the reporting authors,
but no abnormal vessels were demonstrated at angiography. These cryptic VMs were thought to have been
destroyed at the time of hemorrhage. In 15 patients
(23%), hypertension may have been a contributing factor . Two patients had mildly prolonged prothrombin
times due to alcoholic liver disease, and their hemorrhages may have been secondary to a bleeding diathesis .
For 24 patients (360/c ), no cause was apparent (Table 1) .
For one of the patients with an unknown etiology for
the hemorrhage, the reporting authors suspected an infarct that then became hemorrhagic [41 . There is no
radiologic proof of this ; however, it offers another possible mechanism of midbrain hemorrhage .

Spontaneous Midbrain Hemorrhage

Surg Neurol
1993 ;39 :58-65

Table 1 . Cause of Spontaneous Midbrain Hemorrhage
Literature cases Mayo cases Combined series
Cause
(n = 66)
(n = 7)
(n = 73)
Documented VM
10
Presumed VM
15
Hypertension
15
Unknown
24
Clotting
2
disturbance
Abbreviation : Vii, vascular malformation .

2
0
0

12
15
15
27

Of the seven patients in our series, case 3 had an
AVM identified by angiography and visualized at operation . Case 7 had multiple intracranial cavernous malformations ; one was in the midbrain and was the cause of
her SMH . For cases 2, 4, and 5, no cause was apparent .
Case 2 also had hypertension, but his chronic course was
inconsistent with a hypertensive bleed . Two patients
were on anticoagulants at the time of hemorrhage . Case
1 was on warfarin and had a markedly prolonged prothrombin time as well as a questionable history of hypertension . Heparin anticoagulation was suspected to be the
main contributing factor for the midbrain hemorrhage in
case 6 (Table 1) . One of our patients (case 7) and one
from the literature [29] were pregnant at the time of
SMH ; both had VMs . Pregnancy has been reported to
be associated with an increased risk of VM rupture [591 .
Rupture of a VM is a commonly proven or proposed
mechanism of SMH . Angiographically visible VMs of
the posterior fossa are relatively rare and represent 5
to 16% of all intracranial VMs in several clinical series
[3,42,61] . Similarly, Lobato et al [321 reviewed 260
angiographically occult VMs and found that 34 (13%)
were infratentorial, three of which (1 %) were located in
the midbrain . In contrast, McCormick and Nofzinger
[351 found 147 (48%) of 308 "cryptic" VMs were infrarentorial, with 85 (28%) being located in the brain stem .
Abe et al [1) reported a series of 63 brain-stem VMs,
half of which were angiographically occult and diagnosed
only by CT or MRI brain scanning . It remains possible
that very small (1- to 2-mm) VMs located in the midbrain
might not be demonstrated on a prehemorrhage imaging
study (if one is obtained) and are not seen after bleeding
because they are obliterated, substantially reduced in
size, or overshadowed by the accompanying hemorrhage . Although the existence of such small VMs remains speculative, they may occur and are likely to be
responsible for at least some cases of SMH .

Comparison of Major Etiologic Groups

The location of the bleeding in the midbrain was compared in VM-related hemorrhages and those likely due

61

Table 2. Age and Sex of Patients with Spontaneous Midbrain
Hemorrhage

Literature cases

Mayo cases

Combined series

(a = 66)"

(n = 7)-

(n = 69)

Age range
3 mo to 71 yr 30 to 87 yr 3 mo to 87 yr
Sex distribution
37M/25F
4MI3F
41M/28F
Average age (yr)
46
59
47
Median age (yr)
49
55
49
- Information available for only 62 of 66 Literature cases .

to hypertension . Among the 12 patients with documented VMs, the bleeding was localized to the tectum
in four 17,54,57 and patient 3 in this study] and the
tegmentum in five [14,21,27,29 and patient 7 in this
study], with extension into the third ventricle in two of
the latter cases (21,271 ; involved the tectum and tegmentum in two [1,12] ; and was isolated to the peduncle
in one case [451 . Of the 15 patients with a history of
hypertension, one had bleeding isolated to the rectum
[60] ; nine had hemorrhage primarily in the tegmentum
[12,16,20,36-38,41,43,561, four of whom also had extension into the third ventricle [12,36,37,431 ; two had
involvement of the rectum and tegmentum [10,431 ; one
had involvement of the tegmentum and peduncle [101 ;
and two had bleeding isolated to the cerebral peduncle
[39,46] . Although a greater percentage of hemorrhages
from VMs were isolated to the rectum (33% compared
with 7%), no further definite conclusions can be drawn
from the overall comparison about differences in predilection for location between VM-related hemorrhages
and those attributed to hypertension .
The average age of the patients with V M-related hemorrhages was 34 years, whereas it was 58 years for those
with hypertension-associated bleeding .
The outcomes were similar for both etiologic groups :
most recovered with mild or no deficits (82% in VMrelated hemorrhage, 67 % in hypertensive bleeding), and
one patient from each group died .

Clinical Presentation

In the literature cases, patient ages ranged from 3 months
to 71 years . There was a male predominance (3 :2) in
the 62 cases in which sex was reported . All six of the
patients under age 19 years were male . The patients in
our series ranged in age from 30 to 87 years ; four were
men and three were women (Table 2) .
Various clinical syndromes related to lesions of the
midbrain have been described including Webei s,
Benedikt's, Claude's, Nothnagel's, and Parinaud's syndromes . In the cases reported here and those in the
literature, identifiable midbrain syndromes were rare .
Because of the complex anatomy of the midbrain, a

62

Surg Neurol
1993 ;39 :58-65

multitude of neurologic signs and symptoms can result
from even a small lesion . A few patients have had classic
findings .
Roig et al [43] described a patient with Claude's syndrome evolving into Benedikt's syndrome . One of
Weisberg's [58] patients had findings consistent with
Benedikt's syndrome and another had Weber's syndrome . Gaymard et al [18] also described a patient with
Weber's syndrome . Two cases of Nothnagel's syndrome
have been reported (22,47) . Three cases of SMH causing pure sensory stroke have been reported [2,56,57] .
There have been three cases of SMH causing an isolated
nerve III palsy as the only clinical manifestation
[28,48,49] . In three patients, peduncular hallucinosis
developed secondary to SMH [21,43,58] . Ono and Inoue [41] described a patient with cheiro-oral syndrome
(sensory disturbance of the corner of the mouth and
palm of the ipsilateral hand) . Miyashita et al [38] reported a case of vertical one-and-a-half syndrome (bilateral upgaze palsy and monocular paresis of downgaze) .
Thus, the presentation of SMH is variable with regard
to neurologic findings. Neuro-ophthalmologic abnormalities relating to cranial nerve III and/or IV were the
most frequent findings, being present in 58 (88%) of the
66 cases in the literature . Conjugate upward gaze paresis
was present in 33 (57%) of these 58 . This may be the
single most helpful diagnostic finding for localizing the
lesion to the midbrain . Disturbance of consciousness,
often transient and ranging from somnolence and lethargy to coma, was present in 33 patients (50%) . Headache, with or without nausea and vomiting, was noted in
34 patients (52%) ; it frequently was the initial symptom
of the midbrain hemorrhage. Corticospinal tract deficits
were present in 32 patients (48(7o); 22 of these 32 also
had evidence of corticobulbar involvement, with dysarthria being present in 14 . Twenty-one patients (32%)
had lost one or more sensory modalities, usually contralateral to the site of the hemorrhage if the hemorrhage
was lateralized . Twenty-two (33%) of the 66 patients
had an ataxic gait . Two patients had tinnitus and one
patient experienced hyperacusis, suggesting involvement of the inferior colliculus (Table 3) .
Of the seven patients in our series, six had abnormalities of cranial nerve III or IV : two (cases 4 and 5) had
nerve IV palsies as their only abnormality of eye movement, and four had evidence of nerve III involvement .
Cases 6 and 7 had conjugate paralysis of upward gaze
out of proportion to their nerve III deficits . In six of the
seven patients in our series, some degree of alteration
of consciousness developed . Two patients (cases 1 and
5) experienced sudden loss of consciousness as the first
manifestation of their SMH . Four patients (cases 3, 4, 5,
and 7) reported headache associated with their SMH,
but it was not prominent or lasting (Table 3) .

Link et al

Table 3 . Clinical Findings in Patients with Spontaneous
Midbrain Hemorrhage
(n = 66)

Mayo cases
(n = 7)

Combined series

Finding

Literature cases
Cranial nerve 111
or IV paresis
Disturbance of
consciousness
Headache
Corricospinal
tract deficits
Corricobulbar
deficits
Hemisensory
deficits
Gait araxia
Visual hallucinations
Tinnims or
hyperacusis

58

6

64

33

6

39

34
32

(n = 73)

38
36

22*

2

24

21

3

24

22
3

2
0

24
3

3

2

5

' One patient had corticobulbar deficit without a corricospinal deficit.

The temporal profile of brain hemorrhage usually is
acute, with signs and symptoms reaching a peak within
24 hours . This occurred in 43 (65%) of the 66 SMH
cases in the literature- Sixteen (24%) of the literature
cases followed a subacute course (1 day to 1 month), and
seven (1170) had a chronic course (greater than 1 month)
(Table 4). When a complete description was given, many
of the cases with apparent subacute or chronic temporal
profiles actually had a stepwise progressive course .
Five of the seven patients with SMH in our series had
a single acute event . One patient (case 7) had multiple
acute episodes over several months, and another (case
2) may have had multiple acute hemorrhages that presented as a slowly progressive course (Table 4) . The
frequency with which temporal profiles other than acute
occurred in the literature cases (23 of 66 cases, 35%)
and cases 2 and 7 in our series suggests that often several,
small, nonfatal hemorrhages can occur before the diagnosis of SMH is made .

Table 4 . Clinical Presentation in Patients with Spontaneous
Midbrain Hemorrhage
Literature cases

Mayo cases

Combined series

Presentation

(n = 66)

(a = 7)

(n = 73)

Acute onset
(peak in 24 h)
Subacute onset
(peak I d to
1 mo)
Chronic course
(onset > I mo)

43

5

48

16

0

16

7

2

9

Surg Neurol
1993 ;39 :58-65

Spontaneous Midbrain Hemorrhage

Diagnosis and Differential Diagnosis
CT and MRI are rapid, noninvasive, accurate methods
for diagnosing SMH (Figures 1 and 2) . Since it became
widely available in the mid-1970s, CT has been 100%
successful in the cases reported . That is, no lesion has
been identified by another imaging modality or at operation or autopsy that was missed by CT . Although CT is
preferred for detecting acute hemorrhage, MRI is more
useful for following the evolution of a hemorrhage . MRI
also may reveal an angiographically occult VM
[ 19,3 1,401 and should be performed on all patients with
SMH .
Prior to the performance of a CT or MRI scan, the
diagnosis of SMH often is not considered or the lesion
is misdiagnosed . Three cases have been reported in
which the initial diagnosis was multiple sclerosis, indicating that SMH can follow a remitting and relapsing course
[1,22,46] . Humphreys [23) initially diagnosed a left supratentorial mass in his patient who had a midbrain hemorrhage . Preoperatively, La Torre et al [54) expected to
find a hemorrhagic tumor of the quadrigeminal plate . In
one of the cases reported by Dhopesh et al [10], the
diagnosis was hypertensive encephalopathy before CT
revealed the hemorrhage . In another of the Dhopesh et
al cases and in a case reported by Brismar et al [5), the
diagnosis was midbrain infarction . In the majority of
cases reported in the literature, the clinical presentation
and examination suggested a vascular lesion that was
correctly localized to the midbrain .

Treatment
In most cases of SMH, conservative, supportive treatment is sufficient to ensure a good outcome . If hydrocephalus is present, a diversionary shunting procedure
can be lifesaving, as in seven of the literature cases (in
two of these, surgical exploration also was performed) .
Mangiardi and Epstein [34) and Kashiwagi et al [26)
recommended surgical exploration for documented
brain-stem vascular malformations with a progressive
course . Of note, the majority of the hemorrhages they
referred to were in the pons . Lobato et al [32) suggested
that every intracranial angiographically occult VM that
caused clinical symptoms should be resected, irrespective of location . They did not make a distinction between
cases with hemorrhage and those without .
Seven of the SMH cases in the literature underwent
surgical exploration of the midbrain . In five of these,
clotted blood was evacuated, and in two, the exploration
was negative ; a shunting procedure was performed in
one case in each of these groups . The outcome was good
in six of these seven cases ; one patient died 2 days
postoperatively (in this last case, the exploration had

63

Table 5 . Interventions in Spontaneous Midbrain Hemorrhage
Literature cases Mayo cases Combined series
Intervention
(n = 66)
(n = 7)
(n = 73)
Exploration
with
evacuation of
clot
Surgical
exploration
without
evacuation of
clot
Total shunting
procedures

5 (t also shunted)

0

5

2 (1 also shunted)

1

3

7

0

7

been negative and ventriculocisternal shunting had been
performed) [14}. Thus, all five patients who underwent
successful surgical evacuation improved postoperatively .
Five other patients had diversionary shunts only and had
improvement in their neurologic status (Table 5) .
Case 3 in our series had an unsuccessful attempt to
remove her midbrain AVM and hematoma (Table 5) .
Obliteration of the AVM was then performed by stereotactic gamma knife radiosurgery . Gamma knife radiosurgery is a promising new treatment option for deep-seated
VMs [33] . The remaining six patients in our series received only supportive treatment for their SMH .
Outcome
The course of SMH can be surprisingly benign . In 16
(24%) of the 66 reported cases in the literature, the
neurologic findings were normal at follow-up . In the
majority of the literature cases (35 patients, 53%%), relatively minor neurologic deficits persisted, related chiefly
to cranial nerve III or IV, or both . All the patients
with minor neurologic deficits were able to return to
independent living . In 10 cases (159b), moderate neurologic deficits persisted and the patients required longterm care . Three patients (5%) died, and for two, no
follow-up was available (Table 6) . The mean duration of

Table 6. Outcome in Spontaneous Midbrain Hemorrhage
Literature cases Mayo cases Combined series
Outcome
(e = 66)
(n = 7)
(n = 73)
Normal
Mild neurologic
deficits
Moderate to
severe
deficits
Death
No follow-up

16
35

1
2

17
37

10

2

12

3
2

1

4
3

64

Surg Neurol
1993 ;39 :58-65

follow-up was 9 .4 months for the 66 patients in the
literature (range 0 to 87 months) .
Case 4 in our series was neurologically normal at
follow-up. Two patients (cases 3 and 5) continued to
experience mild abnormalities of extraocular movements as their chief complaint . Cases 6 and 7 required
nursing home placement following hospitalization for
SMH. Patient 1 in our series died shortly after admission, and no follow-up could be obtained for case 2
(Table 6) . Mean follow-up was 22 .1 months for our
series (range 0 to 53 months) .
Two patients in our series who had a poor outcome
(cases I and 6) were on anticoagulants at the time of
their hemorrhage, which no doubt contributed to the
extent of their bleeding . In two of the literature cases,
the prothrombin time was mildly prolonged ; one of
these patients had a large hemorrhage [10,36] . An anticoagulated state at the time of hemorrhage may predispose to a worse outcome.
There were no instances of subsequent hemorrhage
among the patients who presented acutely with SMH .
However, the duration of follow-up in these cases usually was a matter of weeks to months .

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