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Coronal T2WI

Axial GRE showing left pontine cavernoma

Axial T2WI showing left inferior olivary nucleus hypertrophy and altered signal

Sagittal T2WI

Hypertrophic olivary degeneration is a form of transsynaptic degeneration. It represents the end result of a lesion that damages the neuronal connections between the dentate nucleus of the cerebellum, the red nucleus, and the inferior olivary nucleus: the dentatorubral-olivary pathway (1,2). It is considered a unique type of degeneration because it is associated with enlargement, rather than atrophy, of the affected structure—the inferior olivary neurons (3).

The affected circuit connects the dentate nucleus of the cerebellum, the contralateral red nucleus, and the ipsilateral inferior olivary nucleus. The dentate nucleus and the contralateral red nucleus are connected by the superior cerebellar peduncle (dentatorubral tract), with fibers crossing in the decussation of the peduncle at the lower midbrain. This tract is part of a reflex arc that controls fine voluntary movements. The red nucleus and the ipsilateral inferior olivary nucleus are connected by the central tegmental tract. These dentatorubral-olivary connections were described by Guillain and Mollaret (2) in 1931 as the anatomic connections related to palatal myoclonus, which is a common clinical association, and this pathway is thus referred to as the “Guillain-Mollaret triangle.”

In 1935, Trelles (4) reported that isolated lesions of the inferior cerebellar peduncle never cause palatal myoclonus, since anatomically there are no direct connections between the inferior olivary nucleus and the contralateral dentate nucleus. Fibers from the inferior olivary nucleus instead project first to the cerebellar cortex (olivocerebellar tracts) and then to the dentate nucleus. He described these connections as the dentatorubral-olivary pathway (5).

Since hypertrophic olivary degeneration occurs owing to interruption of the pathways composing the Guillain-Mollaret triangle, it most commonly occurs following development of focal lesions of the brainstem. Focal brainstem insults that may lead to pathway interruption include ischemic infarction, demyelination, and hemorrhage, the latter often related to hypertensive disease or diffuse axonal injury following severe head trauma (6–8). Olivary hypertrophy is not seen immediately after the brainstem insult but typically appears in a delayed fashion, usually within 4–6 months. The pathologic process persists and is frequently visible after 10 months. Clinical symptoms such as abnormal movement rarely improve. Although olivary hypertrophy typically resolves in 10–16 months, olivary hyperintensity on T2-weighted images may persist for years after resolution of the hypertrophy (9,10).

The specific relationship between the primary lesion and the development of olivary degeneration results in the production of one of three patterns that are easily understood by reviewing a diagram of the involved neuronal pathway (Fig 3). When the primary lesion is limited to the central tegmental tract, olivary hypertrophy is ipsilateral, since only ipsilateral fibers are affected. When the primary lesion is in the dentate nucleus or in the superior cerebellar peduncle, olivary degeneration is contralateral; and when the lesion involves both the central tegmental tract and the superior cerebellar peduncle, olivary hypertrophy is bilateral. The patient in this case has only unilateral olivary hypertrophy, despite having some signal intensity abnormality in the superior cerebellar peduncle—hypointensity in the tegmental area extends into the left superior cerebellar peduncle.Transneuronal degeneration occurs only from a lesion that results in disconnection of the pathway. Abnormal changes in signal intensity on MR images do not necessarily define the severity of the injury. In this case, the hypointensity on T2-weighted images in the superior cerebellar peduncle does not represent disruption of fibers; instead, it most likely represents staining of adjacent tissues by blood products at the periphery of the pontine hemorrhage.

Olivary enlargement corresponds pathologically to an unusual vacuolar degeneration of cytoplasm that results in enlargement related in part to an increased number of astrocytes. Vacuolar degeneration of the cytoplasm occurs at 6–15 months, and gliosis follows 15–20 months after the onset of the primary lesion (10).

Clinical findings associated with olivary hypertrophy include the signature syndrome: palatal myoclonus, or cyclic jerk of the soft palate, and also dentatorubral tremor and ocular myoclonus. Palatal myoclonus, a form of “segmental” myoclonus, is a rhythmic involuntary movement of the oropharynx, similar to the accessory respiratory reflex seen in fish. The typical tremor consists of muscle contractions at one to three cycles per second and is not affected by voluntary controls. Severe myoclonus may also affect the cervical muscles and the diaphragm. The anatomic correlation is the central tegmental tract, which has several connections to the nucleus ambiguus—the vagus nerve is involved in control of palatal movement (5). A lesion in the dentatorubral pathway may cause the patient to lose inhibitory control transmitted through these structures, and palatal myoclonus or other types of abnormal movement may develop. Palatal myoclonus usually develops 10–11 months after the primary lesion, although palatal myoclonus does not always accompany olivary hypertrophy, as is evidenced in the test case (12–14). It should be noted that the clinical pattern of palatal myoclonus also may be seen with focal spinal cord insults (15).

Considering the differential diagnosis of the medullary lesion, high intensity in the anterolateral part of the medulla is not a specific imaging finding. It may be seen with a wide variety of pathologic processes, including infarction; demyelination related to multiple sclerosis; tumor (eg, astrocytoma, metastasis, and lymphoma); and infectious and other inflammatory processes such as tuberculosis, acquired immunodeficiency syndrome, sarcoidosis, and rhombencephalitis. However, if the lesion is strictly limited to one or both inferior olivary nuclei, with sparing of the surrounding medullary tissues, and particularly if there is associated focal olivary enlargement, hypertrophic olivary degeneration should be strongly suggested.

Most neoplasms and infectious processes would be expected to demonstrate intense enhancement. Most infarctions of the medulla are related to disease of the posteroinferior cerebellar artery and are posterolateral in location, or they are related to perforating branches from anterior spinal or vertebral arteries and have a paramedial location. Clinically, acute infarction of the inferior olivary nucleus would likely cause ataxia. Therefore, the diagnosis of infarction is unlikely. Wallerian degeneration, adrenoleukodystrophy, and amyotrophic lateral sclerosis also may demonstrate anterior medullary high intensity on T2-weighted images; however, in these cases, lesions generally are limited to the corticospinal tract and not to the inferior olivary nucleus.

The most important clue to the diagnosis is the association of a remote lesion. The presence of an olivary lesion in association with another lesion in the contralateral cerebellar dentate nucleus, the contralateral superior cerebellar peduncle, the ipsilateral dorsomedial red nucleus, or the ipsilateral pontine tegmentum (as in the test case) makes any diagnosis other than hypertrophic olivary degeneration highly unlikely.

Several authors (16,17) have noted that Wernicke-Korsakoff syndrome may be associated with pathologic change in the inferior olivary nucleus. Again, it is the combination of the inciting lesion in the proper anatomic location, and the observers' knowledge of the association, that permits the diagnosis to be made. MR imaging, due to its exquisite contrast sensitivity and lack of bone artifact in the low posterior fossa, is the most sensitive and specific tool for the diagnosis of olivary hypertrophic changes.

Diagram showing the anatomy involved

1, Thalamus; 2, red nucleus;3, superior cerebellar peduncle; 4, central tegmental tract; 5, dentate nucleus; 6, olivary nucleus; 7, cerebellum.

References

1. ↵ 
   Oppenheim H. Uber oliven degeneration bei atheromatose der basalen hinarterien. Berl Klin Wochenschr 1887; 34:638-639.
2. ↵ 
   Guillain G, Mollaret P. Deux cas de myoclonies synchrones et rhythmes velopharyngo-laryngo-oculo-diaphragmatiques. Rev Neurol 1931; 2:545-566.
3. ↵ 
   Duchen LW. General pathology of neurons and neuralgia. In: Greenfield H, Corsellis JA, Duchen LW, eds. Neuropathology. 5th ed. New York, NY: Wiley,1994; 20-21.
4. ↵ 
   Lapresle J. La voie dento-olivaire: sa mise en evidence, son trajet, sa signification. Bull Acad Natl Med 1984; 168:336-341.

    

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5. ↵ 
   Trelles JO. Les myoclonies vélo-palatines: considération anatomiques et physiologiques. Rev Neurol 1968; 119:165-171.

    

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6. ↵ 
   Gautier JC, Blackwood W. Enlargement of the inferior olivary nucleus in association with lesions of the central tegmental tract or dentate nucleus.Brain 1961; 84:341-364.

    

   FREE Full Text
7. Birbamer G, Gerstenbrand F, Aichner F, et al. MR imaging of post traumatic olivary hypertrophy. Funct Neurol 1994; 9:183-187.

    

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8. ↵ 
   Kitajima M, Korogi Y, Shimomura O, et al. Hypertrophic olivary degeneration: MR imaging and pathologic findings. Radiology 1994; 192:539-543.

    

   Abstract/FREE Full Text
9. ↵ 
   Uchino A, Hasuo K, Uchida S, et al. Olivary degeneration after cerebellar or brain stem hemorrhage: MRI. Neuroradiology 1993; 35:335-338.

    

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10. ↵ 
    Goto N, Kaneko M. Olivary enlargement: chronological and morphometric analysis. Acta Neuropathol (Berl) 1981; 54:275-282.

     

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11. Nieuwenhuys R, Voogd J, Vanhuijzen C. The human central nervous systemNew York, NY: Springer-Verlag, 1988; 230.
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    Matsuo F, Ajax ET. Palatal myoclonus and denervation supersensitivity in the central nervous system. Ann Neurol 1979; 5:72-78.

     

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13. Robin JJ, Alcala H. Olivary hypertrophy without palatal myoclonus associated with a metastatic lesion to the pontine tegmentum. Neurology 1975; 25:771-775.

     

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14. ↵ 
    Bonduelle M. The myoclonias. In: Vinken PJ, Bruyn GW, eds. Handbook of clinical neurology. Vol 6, Diseases of the basal ganglia. New York, NY: Wiley, 1968; 761-781.
15. ↵ 
    Wilkins DE. Myoclonus. In: Samuels MA, Feske S, eds. Office practice of neurology. New York, NY: Churchill-Livingstone, 1996; 686.
16. ↵ 
    Torvik A. Topographic distribution and severity of brain lesions in Wernicke's encephalopathy. Clin Neuropathol 1987; 6:25-29.

     

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    Malamud N, Skillicorn SA. Relationship between the Wernicke and Korsakoff syndrome. Arch Neurol Psychiatry 1956; 76:585-596.

    Abstract/FREE Full Text

He had thick hypertrophied soft palate with persistent myoclonus.......video will be posted next....

Spinal vascular malformations are rare entities and misunderstood

The latest edition of AJNR (Nov-Dec 2010) has two poignant and very important articles in it
see AJNR -- Table of Contents (31, [10])
1st article I recommend is
A.C. Mamourian, H. Young, and M.F. Stiefel
Cumulative Radiation Dose in Patients Admitted with Subarachnoid Hemorrhage:
 A Prospective Study Using a Self-Developing Film Badge 
AJNR Am J Neuroradiol 2010 31: 1787-1790 originally published online on July 1 2010, 10.3174/ajnr.A2192 . [Abstract] [Full Text] [Figures Only] [PDF]  
The cumulative radiation to SAH patient is very high with serial CT scans, diagnostic angiograms
 (CTA/DSA), coiling, chest radiographs etc.
The authors have given a value of upto 1.8 Gy, however in practice, in may instances this is sure
 to exceed especially
if redo interventions, interventions for vasospasm and repeated check angiograms are needed.
From 3 Gy onwards, depilation starts, at 2 Gy erythema starts, and out doses are not very from
 this value.
There has to be more better techniques for reducing the dosage during these procedures.
However, till the technology is not available, we must be very selective and careful in our usage
 of x-ray based machines.


2nd  article is
P. Jun, N.U. Ko, J.D. English, C.F. Dowd, V.V. Halbach, R.T. Higashida, M.T. Lawton, and S.W. Hetts
Endovascular Treatment of Medically Refractory Cerebral Vasospasm Following Aneurysmal Subarachnoid Hemorrhage
AJNR Am J Neuroradiol 2010 31: 1911-1916 originally published online on July 8 2010, 10.3174/ajnr.A2183 . [Abstract] [Full Text] [Figures Only] [PDF]  




SAH leads to vasospasm in 25-30% patients, and leads to prolonged morbidity and poor neurological outcome
 and even death in few.
Traditional treatment with Triple H therapy is helpful many a times, however, endovascular treatment is needed
 sometimes.
The authors have discussed in detail this very important component of SAH management.


Another article in this edition also discusses usage of intra arterial verapamil for vasospam treatment.

June 2010 issue of Radiology has published a very significant article, that with wide-ranging implications.
CECT requests are rampant without any definite indications as most studies can be completed without contrast and studies needing contrast usually also need an MRI scan later; so why not dispense with it altogether.

The authors, Loh et al have found 14.3 % patients developing delayed reactions after CECT using Iohexol, which is definitely very high and probably unaccetable.


Delayed Adverse Reaction to Contrast-enhanced CT: A Prospective Single-Center Study Comparison to Control Group without Enhancement

Shaun Loh , MD , MBA
Sepideh Bagheri , MD
Richard W. Katzberg , MD
Maxwell A. Fung , MD
Chin-Shang Li , PhD
Radiology: Volume 255: Number 3—June 2010


Purpose: To prospectively assess the incidence of delayed adverse reactions (DARs) in patients undergoing contrast material–enhanced computed tomography (CT) with the low osmolar nonionic contrast agent iohexol and compare with the incidence of DARs in patients undergoing unenhanced CT as control subjects.
Materials and Methods:
Institutional review board approval and informed written consent for this prospective study were obtained. The study was HIPAA compliant. Patients undergoing CT for routine indications were enrolled from a random next-available scheduling template by an on-site clinical trials monitor. All subjects received a questionnaire asking them to indicate any DAR occurring later than 1 hour after their examination.
Sixteen manifestations were listed and included rash, skin redness, skin swelling, nausea, vomiting, and dizziness, among others. To ensure maximal surveillance, a clinical trials coordinator initiated direct telephone contact for further assessment. Patients suspected of having moderately severe cutaneous reactions were invited to return for a complete dermatologic clinical assessment including skin biopsy, if indicated.
Statistical analysis was performed by using a twosided Wilcoxon-Mann-Whitney test, a logistic regression
utilizing a x 2 test to adjust for sex and age, and a two- sided Fisher exact test.
Results: A total of 539 patients (258 receiving iohexol and 281 not receiving contrast material) were enrolled. DARs were observed in 37 (14.3%) of 258 subjects receiving iohexol and in seven (2.5%) of 281 subjects in the control group ( P , .0001, x 2 test) after adjusting for sex and age. Specifi c manifestations of DARs that were signifi cantly more frequent at contrast-enhanced CT were skin rash ( P = .0311), skin redness ( P = .0055), skin swelling ( P = .0117), and headache ( P = .0246). DARs involving the skin included generalized
rashes of the face, neck, chest, back, and extremities and were often associated with swelling, erythema, and pruritus.
Conclusion: This study substantiates a frequent occurrence of DARs at contrast-enhanced CT compared with that in control subjects. Continued growth in the use of contrast-enhanced CT suggests a need for greater awareness and attention to prevention and management.
q RSNA, 2010
Supplemental material: http://radiology.rsna.org/lookup
/suppl/doi:10.1148/radiol.10091848/-/DC1


Download
http://www.mediafire.com/?jzkbz3zwzdt

Posterior cerebral artery aneurysms have been managed many a times conservatively.
However, in reality little really solid literature exists as to the subject
Here is a good review of the topic, and according to it endovascular management is the best option among all the three

Download powerpoint from this link
http://www.mediafire.com/?ek2nm5wwx4b

A 23 years-old man developed severe right sided proptosis a month after sustaining head injury in a road traffic accident.
His right orbit showed severe chemosis, injection with decreased ocular movement; vision had decreased to 6/18 ft.
Left eye was normal.
A DSA showed a direct type CCF with rent  near the posterior genu of internal carotid artery and vigorous antegrade flow into the cavernous sinus and ophthalmic veins.
GOLD BAL 4 balloon was used to occlude the fistula using a MAGIC coaxial system.
Post procedure angiogram showed complete occlusion of the fistula with immediate reduction in proptosis nad chemosis.
At 3 months patient 's appearance was totally normal with normal ocular movements but with vision still at 6/18 ft.

In May 26, 2010 issue of NEJM, the much awaited paper was published, dealing with a well planned trial directly comparing carotid endarterectomy and carotid stenting
The results are not surprising: both are equally efficacious with minimal and comparable complications except that more heart attacks were seen in CEA group and more 'brain attacks' in CS.

Stenting versus Endarterectomy   for Treatment of Carotid-Artery Stenosis

Thomas G. Brott, M.D., Robert W. Hobson, II, M.D.,* George Howard, Dr.P.H.,
Gary S. Roubin, M.D., Ph.D., Wayne M. Clark, M.D., William Brooks, M.D.,
Ariane Mackey, M.D., Michael D. Hill, M.D., Pierre P. Leimgruber, M.D.,
Alice J. Sheffet, Ph.D., Virginia J. Howard, Ph.D., Wesley S. Moore, M.D.,
Jenifer H. Voeks, Ph.D., L. Nelson Hopkins, M.D., Donald E. Cutlip, M.D.,
David J. Cohen, M.D., Jeffrey J. Popma, M.D., Robert D. Ferguson, M.D.,
Stanley N. Cohen, M.D., Joseph L. Blackshear, M.D., Frank L. Silver, M.D.,
J.P. Mohr, M.D., Brajesh K. Lal, M.D., and James F. Meschia, M.D.,
for the CREST Investigators†
10.1056/nejmoa0912321


ABSTRACT
BACKGROUND
Carotid-artery stenting and carotid endarterectomy are both options for treating
carotid-artery stenosis, an important cause of stroke.
METHODS
We randomly assigned patients with symptomatic or asymptomatic carotid stenosis
to undergo carotid-artery stenting or carotid endarterectomy. The primary compos-
ite end point was stroke, myocardial infarction, or death from any cause during the
periprocedural period or any ipsilateral stroke within 4 years after randomization.
RESULTS
For 2502 patients over a median follow-up period of 2.5 years, there was no significant
difference in the estimated 4-year rates of the primary end point between the stenting
group and the endarterectomy group (7.2% and 6.8%, respectively; hazard ratio with
stenting, 1.11; 95% confidence interval, 0.81 to 1.51; P  =  0.51). There was no differen-
tial treatment effect with regard to the primary end point according to symptomatic
status (P  =  0.84) or sex (P  =  0.34). The 4-year rate of stroke or death was 6.4% with stent-
ing and 4.7% with endarterectomy (hazard ratio, 1.50; P  =  0.03); the rates among symp-
tomatic patients were 8.0% and 6.4% (hazard ratio, 1.37; P  =  0.14), and the rates among

asymptomatic patients were 4.5% and 2.7% (hazard ratio, 1.86; P  =  0.07), respectively.
Periprocedural rates of individual components of the end points differed between the
stenting group and the endarterectomy group: for death (0.7% vs. 0.3%, P  =  0.18), for
stroke (4.1% vs. 2.3%, P  =  0.01), and for myocardial infarction (1.1% vs. 2.3%, P  =  0.03).
After this period, the incidences of ipsilateral stroke with stenting and with endar-
terectomy were similarly low (2.0% and 2.4%, respectively; P  =  0.85).
CONCLUSIONS
Among patients with symptomatic or asymptomatic carotid stenosis, the risk of the
composite primary outcome of stroke, myocardial infarction, or death did not differ
significantly in the group undergoing carotid-artery stenting and the group undergo-
ing carotid endarterectomy. During the periprocedural period, there was a higher risk
of stroke with stenting and a higher risk of myocardial infarction with endarterec-
tomy. (ClinicalTrials.gov number, NCT00004732.)

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