Neuroradiology:

Classic neuroimaging findings of nonketotic hyperglycemia on computed tomography and magnetic
resonance imaging with absence of typical movement disorder symptoms (hemichorea-hemiballism)

Hansford et al.

Classic neuroimaging findings of nonketotic
hyperglycemia on computed tomography and magnetic
resonance imaging with absence of typical movement
disorder symptoms (hemichorea-hemiballism)
Barry G. Hansford1*, Dara Albert2, Edward Yang1
1. Department of Radiology, University of Chicago Medicine, Chicago, USA
2. Department of Neurology, University of Chicago Medicine, Chicago, USA
* Correspondence: Barry Glenn Hansford, MD, 1600 S. Prairie Avenue, Unit 803, Chicago, IL 60616, USA
(
barry.hansford@uchospitals.edu)

DOI: 10.3941/jrcr.v7i8.1470

ABSTRACT
While there are broad differential diagnoses for either the clinical finding of
hemichorea-hemiballism or the imaging finding of lateralizing/asymmetric
basal ganglia lesions (hyperdense on computed tomography, hyperintense on
T1 magnetic resonance imaging), the presence of both findings is highly
suggestive of nonketotic hyperglycemia. We present an unusual case of a
patient with vague stroke-like complaints and imaging findings notable for
lateralizing basal ganglia lesions. Laboratory analysis revealed nonketotic
hyperglycemia and neurologic exam failed to elicit any findings of
movement disorder. As far as we know, this is the first published case of a
patient with typical neuroimaging manifestations of nonketotic
hyperglycemia without associated hemichorea-hemiballism (a disorder of
abnormal movements comprised of more proximal, higher amplitude
movements-ballismus and lower amplitude, more distal movements- chorea).
This finding suggests that radiologists should be alert to the possibility of
nonketotic hyperglycemia in patients with asymmetric/lateralizing basal
ganglia lesions even in the absence of a movement disorder.

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Radiology Case. 2013 Aug; 7(8):1-9 ::

CASE REPORT
CASE REPORT
A 42 year-old African American male presented to the
emergency department with a 1 week history of progressively
worsening generalized weakness, lightheadedness and
"cloudiness," as well as diffuse "achy" shoulder and back pain.
Additionally, the patient reported a history of his legs feeling
"wobbly" and falling once during the week prior to
presentation. He eventually presented to the emergency room
out of concern he was suffering a stroke. Pertinent past
medical history included type II diabetes, hypertension and
residual left sided weakness and gait problems from a prior
right pontine infarct which occurred approximately 10 months
prior to the current presentation. The patient had prescriptions
for nifedipine, subcutaneous insulin, folate, and vibramycin.
He did not take neuroleptic medication.
Radiology Case. 2013 Aug; 7(8):1-9

The patient's neurologic exam revealed mild right sided
deficits which were new, including flattening of the nasolabial
fold on the right and a slight right pronator drift, although
significant right sided weakness could not be elicited on
formal strength testing. In addition, there was residual
weakness and hyperreflexia on the left side from his prior
infarct. The remainder of the neurological exam was
unremarkable. Specifically, there was no evidence of
hemichorea-hemiballism (HC-HB), a disorder of abnormal
movements comprised of more proximal, higher amplitude
movements-ballismus; and lower amplitude, more distal
movements-chorea.
Due to concern for acute ischemia, a non-contrast head
computed tomography = (CT) exam was performed in the
emergency department which demonstrated hyperdensity
1

Classic neuroimaging findings of nonketotic hyperglycemia on computed tomography and magnetic
resonance imaging with absence of typical movement disorder symptoms (hemichorea-hemiballism)

within the caudate nuclei and left lentiform nucleus which was
new from a study performed ten months earlier (Figure 1).
Contrast enhanced magnetic resonance imaging (MRI) of the
brain was subsequently obtained within 12 hours of the initial
CT (Figures 2-6) and demonstrated corresponding intrinsic T1
shortening in the left globus pallidus (GP) with contrast
enhancement in the lentiform and caudate nuclei (left much
greater than right) (Figures 4,6). There was also faint fluid
attenuated inversion recovery (FLAIR) signal abnormality in
the GP (left greater than right) and left putamen (Figure 5).
Diffusion weighted imaging was unremarkable apart for some
very faint left putamen restricted diffusion without correlative
FLAIR hyperintensity (FLAIR hyperintensity in the left
putamen did not quite correspond to the site of apparent
diffusion restriction), and there was no abnormality on
susceptibility-weighted
imaging
(SWI)
to
suggest
hemorrhage/blood products (Figures 3,2). Consistent with the
patient's history of prior pontine infarct, the MR demonstrated
the sequela of an old stroke involving the right corticospinal
and corticobulbar tracts from the cerebral peduncle superiorly
through the medulla inferiorly. The basal ganglia (BG)
imaging findings were regarded as highly suggestive of
nonketotic hyperglycemia, even though no movement disorder
was detected on clinical exam. Given the CT findings of
hyperdensity without evidence of hemorrhage on MRI,
subacute infarction with petechial hemorrhage was discarded
as a possible etiology.
Laboratory evaluation was notable for serum glucose of
323 mg/dL and a hemoglobin A1c concentration of 13.1%
(normal values are 60-109 mg/dL and 3.9- 6.1% respectively).
The urine specimen was negative for ketones. Calcium level
was 8.5 mg/dL (normal 8.4-10.2) and magnesium was 1.6
mg/dL (normal 1.6-2.5). Supported by the imaging findings,
these laboratory tests were interpreted as consistent with
nonketotic hyperglycemia in the context of poorly controlled
diabetes. The patient later admitted to non-compliance with his
insulin regimen. His symptoms improved and his neurologic
exam returned to baseline with insulin administration and the
normalization of his serum glucose level. Therefore, the
presumed etiology for his initial neurologic symptoms was a
global neurologic dysfunction secondary to hyperglycemia.
After a four day hospitalization, the patient was discharged in
his usual state of health and instructed to follow-up as an
outpatient.

DISCUSSION
Nonketotic hyperglycemia affects patients with poorly
controlled diabetes mellitus who classically present with the
clinical finding of HC-HB [1]. This is a rare condition with the
largest published case series consisting of only 53 patients.
The majority of reported cases have involved Asians, with a
female to male ratio of 1.76. This condition is thought to occur
most frequently in the elderly, most commonly in the seventh
decade [2].
In the radiology literature, nonketotic hyperglycemia has
been associated with a characteristic appearance of unilateral
or asymmetric lesions of the BG which are typically
contralateral to the side of the patient's presenting symptoms.
Radiology Case. 2013 Aug; 7(8):1-9

Hansford et al.

The most frequently described finding associated with
nonketotic hyperglycemia on non-contrast head CT
examination is a hyperdense putamen and/or caudate nucleus
contralateral to the side of the patient's symptoms [1]. The
most commonly described MRI findings associated with
nonketotic hyperglycemia include high signal intensity BG
lesions on T1-weighted brain MRI on the side contralateral to
patient symptoms. The putamen is almost always involved
with variable additional associated BG lesions. There have
been no reports of isolated involvement of the GP or caudate
nucleus. The T2-weighted findings are much more variable
with the majority of BG lesions described as either hypointense or iso-intense to background normal BG[2]. Relatively
little has been published regarding nonketotic hyperglycemia
and findings on DWI and SWI. A small case series and case
report have demonstrated mild to moderate restricted diffusion
corresponding to the T1-weighted hyperintense BG lesions [35]. On SWI, results have been mixed with some of these cases
demonstrating susceptibility while others have not [3-4]. Most
of the published reports did not use contrast, and those that did
use contrast generally indicate no appreciable enhancement
[5]. However, at least one case report describes BG
enhancement with resolution once the serum glucose level was
corrected [6]. On follow-up MRI, Oh et al reported the
resolution of T1 signal abnormalities in 19 of 22 patients
presenting with nonketotic hyperglycemia, suggesting that the
neuroimaging findings of nonketotic hyperglycemia are
usually reversible with appropriate treatment [2]. When
performed,
nuclear
scintigraphy
has
demonstrated
hypoperfusion in the BG with abnormal MRI/CT signal
characteristics, though in some cases after transient
hyperperfusion [1-2,5].
The etiology of the hyperintense signal observed on T1weighted imaging has been the subject of controversy with
several competing hypotheses proposed to account for these
findings. The most widely promoted hypothesis ascribes the
T1 hyperintensity to the protein hydration layer in the
cytoplasm of swollen gemistocytes (reactive astrocytes) [3,5].
Supporting this hypothesis, Shan et al. reported that a biopsy
of a hyperintense putaminal lesion demonstrated abundant
gemistocytes in a fragment of brain tissue [7]. The most
common alternate hypothesis is that the signal abnormality
represents putaminal petechial hemorrhage [7]. However,
blood products are felt to be a less likely etiology given the
manner in which the T1 hyperintensity respects neuroanatomic
boundaries, lack of consistent positive SWI findings and lack
of expected methemoglobin T2-weighted hyperintense
evolution [3]. Nagai et al. has suggested that demyelination
similar to that seen in diabetic peripheral neuropathy leads to
exchange of myelin-bound and axonal water with resultant T1
shortening [8]. Finally, some have speculated that the T1
shortening reflects transient ischemic changes or desiccation
seen as part of localized Wallerian degeneration [2,4].
It is important to remember that T1-weighted
hyperintensity involving the lentiform nucleus does have a
differential diagnosis, particularly if symmetric/bilateral, and
must be interpreted in the context of the patient's past medical
history, presentation and laboratory values to arrive at the
correct diagnosis. Similar T1-weighted hyperintense findings
2

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Neuroradiology:

Neuroradiology:

Classic neuroimaging findings of nonketotic hyperglycemia on computed tomography and magnetic
resonance imaging with absence of typical movement disorder symptoms (hemichorea-hemiballism)

The typical imaging manifestations of nonketotic
hyperglycemia are closely associated with HC-HB. In the
largest published case series of nonketotic hyperglycemia and
BG lesions, all 53 patients demonstrated either unilateral or
bilateral ballismus-chorea [2]. Mechanistically, this association
with movement disorders is unsurprising as the BG(GP,
putamen, caudate, subthalamic nucleus and substantia nigra)
comprise a functional circuit within the deep grey matter
structures of the cerebral hemispheres which controls
movement through its influence on thalamocortical tracts.
Dysfunction within this circuit will therefore lead to a myriad
of different movement disorders including ballismus (more
proximal, higher amplitude movements) and chorea (lower
amplitude, more distal movements), which often occur
together clinically. While HC-HB, has been classically thought
to most commonly reflect an underlying subthalamic nucleus
lesion on the contralateral side, imaging evidence suggests that
lesions elsewhere in the BG are actually more common in HCHB [12-13]. Other well documented etiologies for HC-HB
include ischemic or hemorrhagic stroke and tumors [12].
Nonketotic hyperglycemia is speculated to cause HC-HB
because it forces cerebral metabolism to shift to the anaerobic
pathway abandoning the Krebs cycle. The brain responds by
using an alternative source of energy which includes the
metabolization of the inhibitory neurotransmitter GABA into
succinic acid. In nonketotic hyperglycemia, GABA and acetate
are rapidly depleted and not readily resynthesized, leading to a
reduction of acetylcholine synthesis as well. It is hypothesized
that limited availability of both acetylcholine and GABA in the
BG, coupled with metabolic acidosis and lack of energy
production, may result in BG dysfunction presenting clinically
as chorea [2]. The reason for selective vulnerability of one
side's BG remains unclear.
Our case of nonketotic hyperglycemia demonstrated the
classic finding of CT hyperdensity and T1-weighted
hyperintensity in the left BG, referable to the side of the
patient's presenting symptoms of mild weakness on the right.
In this case, there was also left side predominant FLAIR signal
increase and enhancement of the BG. On DWI, there was only
faint restricted diffusion in the left putamen. On SWI , the BG
demonstrated no convincing abnormalities. As with prior cases
Radiology Case. 2013 Aug; 7(8):1-9

of nonketotic hyperglycemia, the imaging findings in the BG
conformed to the neuroanatomic boundaries of the caudate
nuclei and left lentiform nucleus without associated mass
effect or edema. Along with the SWI data, this pattern argues
against parenchymal hemorrhage or infarction (infarctions and
hemorrhage typically extend outside the BG into the internal
capsule and incite some mass effect). Follow-up imaging for
our patient was not available to evaluate for residual
enhancement after normalization of serum glucose. However,
the imaging findings in this case are typical of those previously
reported for nonketotic hyperglycemia, and not consistent with
other entities in the differential diagnosis (see table 2).
What makes this case unusual is the absence of chorea or
another movement disorder in association with this
pathognomonic imaging appearance of the BG. Instead, the
patient had a subjective sensation of generalized weakness and
mild right sided weakness on neurologic exam, initially
concerning for a new ischemic insult. There has been a case
report of nonketotic hyperglycemia presenting acutely with
stroke-like symptoms, but even in this report the clinical
presentation included chorea [4]. To the best of our
knowledge, our case is the first in the literature to describe the
classic neuroimaging findings of nonketotic hyperglycemia in
a patient who did not clinically have HC-HB or any other
findings suggestive of a movement disorder. Therefore, this
case suggests that nonketotic hyperglycemia may have a
broader spectrum of clinical presentation than is currently
appreciated even when it has characteristic involvement of the
BG. This observation is concordant with the well-described
phenomenon in neurology that hyperglycemia (as well as
hypoglycemia) can present with global neurologic dysfunction
(encephalopathy and coma) as well as focal neurologic deficits
(hemiplegia, aphasia and seizures) [14].

TEACHING POINT
Nonketotic hyperglycemia should be a diagnostic
consideration even without hemichorea-hemiballismus when
the typical neuroimaging findings are present. This is an
important diagnosis to make as early as possible because the
clinical outcome is excellent with the rapid institution of
appropriate insulin therapy and the radiologist may be the first
to appreciate the importance of the patient's hyperglycemia to
their clinical presentation given the characteristic imaging
appearance.

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8791916
2. Oh SH, Lee KY, Im JH, Lee MS. Chorea associated with
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53 cases including four present cases. J Neurol Sci 2002;
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3

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on neuroimaging have been observed with manganese toxicity
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on non-contrast head CT and intrinsic T1 hyperintensity on
MRI include hemorrhage/blood products and asymmetric
calcification/mineralization including that associated with
underlying lesions such as developmental venous anomalies
[11].

Hansford et al.

Neuroradiology:

Classic neuroimaging findings of nonketotic hyperglycemia on computed tomography and magnetic
resonance imaging with absence of typical movement disorder symptoms (hemichorea-hemiballism)

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BK, Feuerbach S. Tentorial and dural calcification with
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20. Kim TJ, Kim IO, Kim WS, et al. MR imaging of the brain
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4

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Journal of Radiology Case Reports

6. Iwata A, Koike F, Arasaki K, Tamaki M. Blood brain
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PMID: 10223418

Hansford et al.

Neuroradiology:

Classic neuroimaging findings of nonketotic hyperglycemia on computed tomography and magnetic
resonance imaging with absence of typical movement disorder symptoms (hemichorea-hemiballism)

Hansford et al.

Figure 1: 42 year-old male who presented with vague right sided stroke-like symptoms and was found to have nonketotic
hyperglycemia. FINDINGS: (1a) Axial non-contrast computed tomography of the head performed at ten months prior to
current presentation demonstrates no abnormalities at the level of the basal ganglia. TECHNIQUE: Philips 64-slice CT
scanner, 501mAs, 120 kvp, 5mm slice thickness. FINDINGS: (1b) Axial non-contrast computed tomography of the head
performed at time of current presentation demonstrates interval development of hyperdensity within the caudate nuclei (straight
arrows) and left lentiform nucleus (curved arrow) which respects the neuroanatomic boundaries of the basal ganglia without
associated edema. TECHNIQUE: Philips 64-slice CT scanner, 350mAs, 120 kvp, 5mm slice thickness.

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FIGURES

Figure 2: 42 year-old male who presented with vague right sided stroke-like symptoms and was found to have nonketotic
hyperglycemia. FINDINGS: Axial SWI MR images of the brain (2a) at the level of the basal ganglia and (2b) slightly superior
at the level of the atria of the lateral ventricles performed at time of current presentation are unremarkable without basal
ganglia or caudate nuclei blooming to suggest blood products..TECHNIQUE: 1.5T Philips Intera MR scanner, susceptibilityweighted imaging (VEN_BOLD_HR SENSE) sequence, TR=23.60, TE=33.60, no contrast.
Radiology Case. 2013 Aug; 7(8):1-9

5

Classic neuroimaging findings of nonketotic hyperglycemia on computed tomography and magnetic
resonance imaging with absence of typical movement disorder symptoms (hemichorea-hemiballism)

Hansford et al.

Figure 3: 42 year-old male who presented with vague right sided stroke-like symptoms and was found to have nonketotic
hyperglycemia. FINDINGS: (3a) Axial DWI MR image of the brain at the level of the basal ganglia and (3b) axial ADC map
correlate demonstrate faint restricted diffusion confined to the left putamen. TECHNIQUE: (3a) 1.5T Philips Intera MR
scanner, diffusion-weighted imaging (DWI), TR=3873.32, TE=73.10, no contrast and (3b)1.5T Philips Intera MR scanner,
diffusion-weighted ADC map, TR=3873.32, TE=73.10, no contrast.

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Figure 4: 42 year-old male who presented with vague right sided stroke-like symptoms and was found to have nonketotic
hyperglycemia. FINDINGS: Axial pre-contrastT1-weighted MR images of the brain through the basal ganglia and caudate
nuclei from caudal to cranial (4a-c) demonstrate intrinsic T1 shortening confined to the left globus pallidus (arrows),
corresponding to the hyperdensity seen on presenting CT. TECHNIQUE: 1.5T Philips Intera MR scanner, T1-weighted
imaging, TR=586.65, TE=12, pre-contrast. FINDINGS: Axial post-contrast T1-weighted MR images of the brain through the
basal ganglia and caudate nuclei from caudal to cranial (4d-f) corresponding to (4a-c) respectively demonstrate contrast
enhancement respecting the neuroanatomic boundaries of the lentiform (straight arrows) and caudate nuclei (curved arrows)
(left much greater than right). TECHNIQUE: 1.5T Philips Intera MR scanner, fat saturated T1-weighted imaging, TR=595.10,
TE=12, with 18ml of gadodiamide (Omniscan, GE health care, Princeton, NJ) injection.
Radiology Case. 2013 Aug; 7(8):1-9

6

Classic neuroimaging findings of nonketotic hyperglycemia on computed tomography and magnetic
resonance imaging with absence of typical movement disorder symptoms (hemichorea-hemiballism)

Hansford et al.

Figure 5: 42 year-old male who presented with vague right sided stroke-like symptoms and was found to have nonketotic
hyperglycemia. . FINDINGS: Axial FLAIR MR images of the brain at the level of the basal ganglia (5a) slightly caudal to (5b)
demonstrate subtle hyperintense signal abnormalities in the globus pallidi (left greater than right) (arrows). (5b) FLAIR
hyperintense signal abnormality confined to the left putamen (arrow). TECHNIQUE: 1.5T Philips Intera MR scanner, fluid
attenuated inversion recovery imaging (FLAIR), TR=11000, TE=140, no contrast.

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Neuroradiology:

Figure 6: 42 year-old male who presented with vague right sided stroke-like symptoms and was found to have nonketotic
hyperglycemia. FINDINGS: Sagittal T1-weighted pre-contrast MR images of the brain through the basal ganglia and caudate
nuclei (6a) right and (6c,6e) left demonstrates intrinsic T1 shortening confined to the left globus pallidus (arrows).
TECHNIQUE: 1.5T Philips Intera MR scanner, T1-weighted imaging, TR=541.53, TE=12, pre-contrast. Sagittal T1-weighted
post-contrast MR images of the brain through the basal ganglia and caudate nuclei, (6b) corresponding to (6a) on the right and
(6d,f) corresponding to (6c,e) respectively on the left demonstrate contrast enhancement which respects the neuroanatomic
boundaries of the lentiform (straight arrows) and caudate nuclei (curved arrows) (left much greater than right). TECHNIQUE:
1.5T Philips Intera MR scanner, T1-weighted imaging, TR=541.53, TE=12, with 18ml of gadodiamide (Omniscan, GE health
care, Princeton, NJ) injection.
Radiology Case. 2013 Aug; 7(8):1-9

7

Neuroradiology:

Classic neuroimaging findings of nonketotic hyperglycemia on computed tomography and magnetic
resonance imaging with absence of typical movement disorder symptoms (hemichorea-hemiballism)

Etiology:
Incidence:
Gender ratio:
Age predilection:
Risk factors:
Treatment:
Prognosis:
Findings on imaging:

Hansford et al.

Controversial, leading hypothesis states hyperintense T1-weighted signal is secondary to
unwrapping of myelin sheath and swollen gemistocytes [3,5]
Rare; largest published case series consists of 53 patients, majority of reported cases involve Asians
[2]
Of the 53 cases with gender available, 30 females and 17 males (ratio of F to M: 1.76) [2]
Range: 22-92 years, mean age of 71.1 years [2]
History of poorly controlled diabetes mellitus [2]
Normalization of blood glucose levels with appropriate insulin therapy [2]
Excellent with timely instillation of insulin therapy [2]
MR: unilateral or asymmetric T1-weighted hyperintense BG lesion, T2- variable, susceptibility and
diffusion - variable, often enhances [2]

Entity
Imaging Findings: MRI
Physiologic
 Bilateral T1-hyperintense
calcification, normal
BG, GP more than putamen
variant [15]

Imaging Findings: CT
CT: Calcifications in same
distribution as MR

Manganese toxicity  Bilateral T1-hyperintensity
in long term total
in the substantia nigra and
parenteral nutrition
GP, T2- unremarkable
[9]
Disorders of calcium  Bilateral T1-hyperintensity
metabolism [16-17]
BG, T2-hypointense, SWIblooming

CT: Unremarkable

CT: Bilateral BG calcifications

 Bilateral T1-hyperintense
 MR: Bilateral T1BG (especially GP), pituitary
hyperintense BG (especially
GP), pituitary gland, and
hypothalamus
 CT: Unremarkable
Wilson disease [20]  T1 BG signal variable,
MR: T2 “face of giant panda
sign” normal red nucleus on
typically reduced, but may be
background of hyperintense
hyperintense
tegmentum
 T2 “face of giant panda sign”
 Widening of frontal horns,
normal red nucleus on
diffuse brain atrophy
background of hyperintense
tegmentum
 +/- BG hypodensity
Fahr disease [21-22]  BG T1 hyperintense, T2
CT: Extensive symmetric BG
calcifications (especially GP),
variable, SWI- markedly
thalami, cerebellum (dentate
hypointense
nuclei)
Hypoxic brain
CT:
If acute, normal
 BG and cortical hyperintense
changes [23-24]
lesions, DWI- restricted
 After acute phase, decreased
diffusion if acute
bilateral BG attenuation
Neurofibromatosis
CT?: BG unremarkable; optic or
 Foci of T1 and T2
type one [25-26]
parenchymal gliomas may be
hyperintensity in the deep
present; sphenoid wing
gray nuclei (especially GP),
dysplasia
may resolve by adulthood
Chronic liver
disease [18-19]

Clinical Findings
 Seen as normal variant aging
brain, asymptomatic
 Typically in patients older than
30 years
 History of long term total
parenteral nutrition
 Findings secondary to manganese
deposition
 History of 1o or 2o
hyperparathyroidism, 1o or 2o
hypoparathyroidism, or pseudohypoparathyroidism
 History/stigmata of chronic liver
disease
 May present acutely with
jaundice, encephalopathy

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Table 1: Summary table for nonketotic hyperglycemia

 T1 hyperintensity secondary to
deposition of copper
 Liver disease, Kayser-Fleischer
rings
 Decreased ceruloplasmin
 Neuropsychiatric disturbance,
cognitive impairment,
extrapyramidal findings
 Laboratory values normal
 History of anoxia, near-drowning,
hypoxia, and/or cerebral
hypoperfusion injury
 Cutaneous café au lait spots
earliest finding
 Progressive vision loss due to
optic gliomas
 Half of patients have
macrocephaly

Table 2: Differential diagnosis table for basal ganglia signal abnormalities

Radiology Case. 2013 Aug; 7(8):1-9

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Neuroradiology:

Classic neuroimaging findings of nonketotic hyperglycemia on computed tomography and magnetic
resonance imaging with absence of typical movement disorder symptoms (hemichorea-hemiballism)

Hansford et al.

ABBREVIATIONS
BG = basal ganglia
CT = computed tomography
DWI = diffusion-weighted imaging
FLAIR = fluid attenuated inversion recovery imaging
GP = globus pallidus
HC-HB = hemichorea-hemiballism
MRI = magnetic resonance imaging
SWI = susceptibility-weighted imaging

KEYWORDS

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Journal of Radiology Case Reports

Nonketotic hyperglycemia; T1 hyperintense basal ganglia
lesion; hemichorea-hemiballismus

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