tag:blogger.com,1999:blog-1157996001534275622024-03-07T19:45:49.755-08:00NeuroexamBlog on neurological examinationCarlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.comBlogger14125tag:blogger.com,1999:blog-115799600153427562.post-78035406219616649972015-05-11T08:12:00.002-07:002015-05-11T08:12:04.548-07:00Screening Neurological Exam<div class="separator" style="clear: both; text-align: center;">
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<br />Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com0tag:blogger.com,1999:blog-115799600153427562.post-61268556418511970862014-07-19T05:29:00.001-07:002014-07-19T05:29:22.959-07:00Ocular bobbing and dippingOcular bobbing, dipping and floating are not too rare, if you keep examining your comatose and brainstem patients repeatedly. We discuss the few things that are known about these eye movement disorders and relish the wonderful poem of Ross 1992:<br />
<br />
<i><span style="font-family: Trebuchet MS, sans-serif;">You’re called to the bedside, the eye movements are strange.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">There must be a reason, can you give it a name?</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">You’ve seen this before, but can you recall?</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">You’re the Neurologist, you’re supposed to know all!</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;"><br /></span></i>
<i><span style="font-family: Trebuchet MS, sans-serif;">In bobbing and dipping, the eyes go down.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">“How is that?” you ask with a frown.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">The first is brisk, the second is slow.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">The meaning differs; you must know.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;"><br /></span></i>
<i><span style="font-family: Trebuchet MS, sans-serif;">Bobbing suggest pons; dipping an anoxic brain.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">As always, there are some exceptions to name.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">Metabolic encephalopathy can make the eyes bob.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">Cerebellar hemorrhage and trauma complete the log.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;"><br /></span></i>
<i><span style="font-family: Trebuchet MS, sans-serif;">To remember all this, you need something terse.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">But wait, don’t forget, it could be reverse!</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">In each of these cases, it’s up the eyes go.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">Bobbing is fast and dipping is slow.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;"><br /></span></i>
<i><span style="font-family: Trebuchet MS, sans-serif;">Reverse bobbing may be something you see, </span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">again, with metabolic encephalopathy.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">Reverse dipping, a rare clinical nidus,</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">is reported in AIDS with cryptococcal meningitis.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;"><br /></span></i>
<i><span style="font-family: Trebuchet MS, sans-serif;">Despite the confusion, one thing is plain.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">The eyes don’t work right, whatever the name.</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">Wheter bobbing or dipping or reversing is true,</span></i><br />
<i><span style="font-family: Trebuchet MS, sans-serif;">it can’t be good; just be glad it’s not you!</span></i><br />
<br />
I would add that in Bobbing usually the horizontal VOR fails (with calorics or doll’s head maneuver). Here is a link to an article about the stuff<br />
<a href="http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1033087/" target="_blank">The clinical spectrum of ocular bobbing and ocular dipping. JNNP 1988.</a>Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com0tag:blogger.com,1999:blog-115799600153427562.post-33438575778544855742013-10-12T09:25:00.004-07:002013-10-12T09:26:51.114-07:00Medical Research Council (MRC) Scale for Muscle Strength<br />The patient's effort is graded on a scale of 0-5:<br />Grade 5: Muscle contracts normally against full resistance.<br />Grade 4: Muscle strength is reduced but muscle contraction can still move joint against resistance.<br />Grade
3: Muscle strength is further reduced such that the joint can be moved
only against gravity with the examiner's resistance completely removed.
As an example, the elbow can be moved from full extension to full
flexion starting with the arm hanging down at the side.<br />Grade 2:
Muscle can move only if the resistance of gravity is removed. As an
example, the elbow can be fully flexed only if the arm is maintained in a
horizontal plane.<br />Grade 1: Only a trace or flicker of movement is seen or felt in the muscle or fasciculations are observed in the muscle.<br />Grade 0: No movement is observed. <br /><br /><br /><br />Clinical grading scale employed for functional assessments<br />Grade 0: normal.<br />Grade 1: no disability; minor sensory signs or areflexia.<br />Grade 2: mild disability; ambulatory for &gt;200 m; mild weakness in one or more limbs and sensory impairment.<br />Grade 3: moderate disability; ambulatory for &gt;50 m without stick; moderate weakness MRC Grade 4 and sensory impairment.<br />Grade 4: severe disability; able to walk &gt;10 m with support of stick; motor weakness MRC Grade 4 and sensory impairment.<br />Grade 5: requires support to walk 5 m; marked motor and sensory signs.<br />Grade 6: cannot walk 5 m, able to stand unsupported and able to transfer to wheelchair, able to feed independently.<br />Grade 7: bedridden, severe quadriparesis; maximum strength MRC grade 3.<br />Grade 8: respirator and/or severe quadriparesis; maximum strength MRC grade 2.<br />Grade 9: respirator and quadriplegia.<br />Grade 10: dead.<br /><br /><br /><br /><br />Reference:<br />Medical
Research Council. Aids to the examination of the peripheral nervous
system, Memorandum no. 45, Her Majesty's Stationery Office, London,
1981.<br />Hahn AF, Bolton CF, Pillay N, et al. Plasma exchange therapy in chronic inflammatory<br />demyelinating polyneuropathy. A double-blind, sham controlled, cross-over study.<br />Brain 1996;119:1055–66. [Medline]<br />Paternostro-Sluga
T, Grim-Stieger M, Posch M, Schuhfried O, Vacariu G, Mittermaier C,
Bittner C, Fialka-Moser V. Reliability and validity of the Medical
Research Council (MRC) scale and a modified scale for testing muscle
strength in patients with radial palsy. J Rehabil Med. 2008
Aug;40(8):665-71. Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com4tag:blogger.com,1999:blog-115799600153427562.post-9145181079607631112013-04-27T02:22:00.002-07:002013-04-27T02:22:22.351-07:00Conducting a Neurological Examination in English <div class="separator" style="clear: both; text-align: center;">
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<br />Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com0tag:blogger.com,1999:blog-115799600153427562.post-30234403221331455692013-03-26T09:38:00.002-07:002013-03-26T09:38:16.744-07:00 Medical Education de UCD School of Medicine and Medical Science <iframe width="560" height="315" src="http://www.youtube.com/embed/videoseries?list=PLHdemSStztKYUMueSRCRWBuNxqU0Ckr0r" frameborder="0" allowfullscreen></iframe>Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com1tag:blogger.com,1999:blog-115799600153427562.post-53699255740787668192013-01-17T10:06:00.001-08:002013-01-17T10:06:14.237-08:00Bilateral Internuclear Ophthalmoplegia in Multiple Sclerosis<div class="separator" style="clear: both; text-align: center;">
<a href="http://gyazo.com/08cbe3951458c40758b2a0ce4d401f06.png" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="205" src="http://gyazo.com/08cbe3951458c40758b2a0ce4d401f06.png" width="400" /></a></div>
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A 45-year-old man with multiple sclerosis presented with worsening
weakness in his right leg and double vision. Neurologic examination
revealed horizontal diplopia during lateral gaze in both eyes. The
patient had an adduction deficit in the right eye and nystagmus in the
left eye on leftward gaze (Panel A). He also had an adduction deficit in
the left eye and nystagmus in the right eye on rightward gaze (Panel
B). Upward gaze (Panel C), downward gaze (Panel D), and normal primary
position (Panel E) were unremarkable.
Internuclear ophthalmoplegia is characterized by impaired horizontal
eye movement that is caused by a lesion in the medial longitudinal
fasciculus, a fiber tract that rises from the abducens nucleus in the
pons to the contralateral oculomotor nucleus in the midbrain. Lesions in
the medial longitudinal fasciculus result in the failure of adduction
on attempted lateral gaze. Any brain-stem syndrome can interrupt the
medial longitudinal fasciculus and result in impaired horizontal eye
movement, but the most frequent underlying cause is multiple sclerosis.
This patient had internuclear ophthalmoplegia in both eyes due to
demyelinating lesions. Glucocorticoids were administered intravenously,
but the deficits did not resolve. On follow-up at 2 months, the
patient's gait had improved, but the internuclear ophthalmoplegia
remained.</div>
Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com0tag:blogger.com,1999:blog-115799600153427562.post-14861070858336379202012-12-14T08:50:00.001-08:002012-12-14T08:51:38.423-08:00Weber and Rinnè tests<div class="separator" style="clear: both; text-align: left;">
Learn how to assess hearing problems with simple tests </div>
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<br />Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com0tag:blogger.com,1999:blog-115799600153427562.post-50550783146174211632012-12-06T01:03:00.002-08:002012-12-06T01:21:45.853-08:00Chvostek's and Trousseau's Signs<div class="separator" style="clear: both; text-align: center;">
<a href="http://www.nejm.org/na102/home/ACS/publisher/mms/journals/content/nejm/2012/nejm_2012.367.issue-11/nejmicm1110569/production/images/nejmicm1110569_attach_1_jesu_icm1110569_thumb111x111.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="http://www.nejm.org/na102/home/ACS/publisher/mms/journals/content/nejm/2012/nejm_2012.367.issue-11/nejmicm1110569/production/images/nejmicm1110569_attach_1_jesu_icm1110569_thumb111x111.jpg" /></a></div>
<span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #333333; display: inline !important; float: none; font-family: arial, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 18.20833396911621px; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">A 38-year-old man presented to the emergency department with facial paresthesias and upper-extremity muscle cramping. His symptoms were progressive, beginning as mild paresthesias on postoperative day 1 by the time he presented, they had been getting worse for about 24 hours. His medical history was noteworthy only for papillary thyroid carcinoma, for which he had undergone a total thyroidectomy 2 days earlier. Physical examination revealed apparent Chvostek's sign (Figure 1A and<span class="Apple-converted-space"> </span></span><a class="viewType-Layer viewClass-WiderLayer" href="http://www.nejm.org/action/showMediaPlayer?doi=10.1056%2FNEJMicm1110569&aid=NEJMicm1110569_attach_1&area=" style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; border: 0px; color: #006892; font-family: arial, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 18.20833396911621px; margin: 0px; orphans: 2; outline: 0px; padding: 0px; text-align: start; text-decoration: initial; text-indent: 0px; text-transform: none; vertical-align: baseline; white-space: normal; widows: 2; word-spacing: 0px;">Video 1</a><span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #333333; display: inline !important; float: none; font-family: arial, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 18.20833396911621px; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">) and Trousseau's sign (Figure 1B and<span class="Apple-converted-space"> </span></span><a class="viewType-Layer viewClass-WiderLayer" href="http://www.nejm.org/action/showMediaPlayer?doi=10.1056%2FNEJMicm1110569&aid=NEJMicm1110569_attach_1&area=" style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; border: 0px; color: #006892; font-family: arial, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 18.20833396911621px; margin: 0px; orphans: 2; outline: 0px; padding: 0px; text-align: start; text-decoration: initial; text-indent: 0px; text-transform: none; vertical-align: baseline; white-space: normal; widows: 2; word-spacing: 0px;">Video 2</a><span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #333333; display: inline !important; float: none; font-family: arial, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 18.20833396911621px; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">), a result of postsurgical acquired hypoparathyroidism. His total calcium level was 5.8 mg per deciliter (normal range, 8.4 to 10.3) (1.45 mmol per liter [2.1 to 2.6]), his free calcium level was 1.68 mEq per liter (normal range, 2.24 to 2.64) (0.84 mmol per liter [1.12 to 1.32]), and his serum phosphate level was 6.6 mg per deciliter (normal range, 2.7 to 4.5) (2.13 mmol per liter [0.87 to 1.45]). The parathyroid hormone level was 7 pg per milliliter (normal range, 15 to 65). </span><br />
<span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #333333; display: inline !important; float: none; font-family: arial, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 18.20833396911621px; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;"></span><br />
<a name='more'></a><span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #333333; display: inline !important; float: none; font-family: arial, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 18.20833396911621px; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;"><br /></span><br />
<span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #333333; display: inline !important; float: none; font-family: arial, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 18.20833396911621px; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Chvostek's sign is described as the twitching of facial muscles in response to tapping over the area of the facial nerve (</span><a class="viewType-Layer viewClass-WiderLayer" href="http://www.nejm.org/action/showMediaPlayer?doi=10.1056%2FNEJMicm1110569&aid=NEJMicm1110569_attach_1&area=" style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; border: 0px; color: #006892; font-family: arial, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 18.20833396911621px; margin: 0px; orphans: 2; outline: 0px; padding: 0px; text-align: start; text-decoration: initial; text-indent: 0px; text-transform: none; vertical-align: baseline; white-space: normal; widows: 2; word-spacing: 0px;">Video 1</a><span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #333333; display: inline !important; float: none; font-family: arial, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 18.20833396911621px; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">). Trousseau's sign is carpopedal spasm that results from ischemia, such as that induced by pressure applied to the upper arm from an inflated sphygmomanometer cuff (</span><a class="viewType-Layer viewClass-WiderLayer" href="http://www.nejm.org/action/showMediaPlayer?doi=10.1056%2FNEJMicm1110569&aid=NEJMicm1110569_attach_1&area=" style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; border: 0px; color: #006892; font-family: arial, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 18.20833396911621px; margin: 0px; orphans: 2; outline: 0px; padding: 0px; text-align: start; text-decoration: initial; text-indent: 0px; text-transform: none; vertical-align: baseline; white-space: normal; widows: 2; word-spacing: 0px;">Video 2</a><span style="-webkit-text-size-adjust: auto; -webkit-text-stroke-width: 0px; background-color: white; color: #333333; display: inline !important; float: none; font-family: arial, sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: 18.20833396911621px; orphans: 2; text-align: start; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">). Chvostek's sign is neither sensitive nor specific for hypocalcemia, since it is absent in about one third of patients with hypocalcemia and is present in approximately 10% of persons with normal calcium levels. Trousseau's sign, however, is more sensitive and specific; it is present in 94% of patients with hypocalcemia and in only 1% of persons with normal calcium levels. Our patient's symptoms resolved with intravenous administration of calcium gluconate, and he was discharged with instructions to begin oral calcium supplementation and to maintain close follow-up with his endocrinologist.</span>Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com0tag:blogger.com,1999:blog-115799600153427562.post-89007134990831604542012-10-15T13:30:00.000-07:002012-10-15T13:30:01.304-07:00Gradenigo syndrome<br />
<div id="p-85">
A 28-year-old woman presented with fever, double vision, and facial pain. Neurologic examination showed neck stiffness, pain
in the distribution of the right trigeminal nerve, and right abducens palsy (<a class="xref-fig" href="http://www.neurology.org/content/79/16/e141.full#F1" id="xref-fig-1-1">figure 1</a>). Tympanic membranes were normal. MRI revealed sphenoid sinusitis, basilar pachymeningitis, and clivus osteomyelitis (<a class="xref-fig" href="http://www.neurology.org/content/79/16/e141.full#F2" id="xref-fig-2-1">figure 2</a>). CSF analysis showed pleocytosis, increased protein contents, decreased glucose levels, and positive cultures for <span class="named-content genus-species" id="named-content-1">Staphylococcus aureus</span>.
The triad of suppurative otitis media, pain in the distribution of the
trigeminal nerve, and abducens palsy is called Gradenigo
syndrome.<sup><a class="xref-bibr" href="http://www.neurology.org/content/79/16/e141.full#ref-1" id="xref-ref-1-1">1</a></sup> While it most often affects children, it may occur in adults and may rarely present without otitis media.<sup><a class="xref-bibr" href="http://www.neurology.org/content/79/16/e141.full#ref-2" id="xref-ref-2-1">2</a></sup> While bone compromise is usually confined to the petrous apex, it may extend to sphenoid sinuses, clivus, and basal meninges.
</div>
<div class="fig pos-float odd" id="F1">
<div class="fig-inline">
<a class="fig-inline-link" href="http://www.neurology.org/content/79/16/e141/F1.expansion.html"><img alt="Figure 1" src="http://www.neurology.org/content/79/16/e141/F1.small.gif" /></a><div class="callout">
<span class="fig-label">Figure 1</span>
<div class="first-child" id="p-86">
Photograph of the patient shows isolated right abducens palsy</div>
</div>
</div>
</div>
<div class="fig pos-float odd" id="F2">
<div class="fig-inline">
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<div class="fig-inline">
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<div class="fig-inline">
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<div class="fig-inline">
<br /></div>
<div class="fig-inline">
<a class="fig-inline-link" href="http://www.neurology.org/content/79/16/e141/F2.expansion.html"><img alt="Figure 2" src="http://www.neurology.org/content/79/16/e141/F2.small.gif" /></a><div class="callout">
<span class="fig-label">Figure 2</span> <span class="caption-title">Head MRI</span>
<div class="first-child" id="p-87">
Contrast-enhanced
T1-weighted MRI of the head shows mucosal thickening of sphenoid sinuses
(arrowheads), basilar and right
middle fossa pachymeningitis (small arrows), and
osteomyelitis of the clivus (large arrow). While the right abducens
nerve
is not well visualized, it could be inferred in
the axial sections (upper row) that it is entrapped throughout the
Dorello
channel and the cavernous sinus.
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<br />Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com0tag:blogger.com,1999:blog-115799600153427562.post-7630627215945738632012-09-16T09:26:00.001-07:002012-09-16T10:02:52.000-07:00Acute Adie syndrome <div class="separator" style="clear: both; text-align: center;">
<a href="http://www.neurology.org/content/79/11/e97/F1.large.jpg" imageanchor="1" style="margin-left: 1em; margin-right: 1em;"><img border="0" height="147" src="http://www.neurology.org/content/79/11/e97/F1.large.jpg" width="400" /></a></div>
Parasympathetic denervation of the iris sphincter muscle in Adie
syndrome results in an enlarged tonic right pupil reacting
poorly to light (A, B). Near response was also
impaired (C). It is supersensitive to cholinergic agents (pilocarpine
0.1%)
(D). Paralysis of the iris results in
characteristic segmental vermiform movements. These are visible
superolaterally acutely
and inferomedially 6 months later Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com0tag:blogger.com,1999:blog-115799600153427562.post-43730308738216928912011-12-28T11:28:00.001-08:002012-12-06T01:04:26.164-08:00Clinical assessment of painSuccessfully treating chronic pain is challenging, as patients respond heterogeneously to analgesic treatments. Such variation in response can be attributed to differing underlying pain-generating mechanisms. A novel clinical bedside test that identifies distinct pain phenotypes might help deliver more-effective mechanism-based treatment strategies.<br />
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Chronic pain is difficult to treat. The analgesic effects elicited by existing drugs are often not satisfactory and patients show differing responses to the available therapies. For both these reasons, there is a need to develop more-effective treatment strategies and pain medications. Heterogeneity in the response to analgesics could be explained by the presence of different underlying pain-generating mechanisms in patients with the same disease. Furthermore, the same pain-generating mechanisms could occur in different conditions, and, in an individual patient, several mechanisms might be present all at once. Scholz et al.<sup><a href="http://jneurology.wordpress.com/article/clinical-assessment-of-pain-23lvr9hhdbqmt-11/#B1">1</a></sup> have developed a novel assessment system for chronic pain to distinguish between different subtypes of pain, and, possibly, distinct underlying pain-generating mechanisms.<br />
Inflammatory pain can be distinguished clinically from neuropathic pain. In the former category, the nociceptive pathways are intact and activated by inflammatory mediators, whereas neuropathic pain develops after a lesion to the nervous system itself. Chronic inflammatory and neuropathic pain are both associated with a cascade of functional, molecular, biochemical and anatomical changes in the PNS and CNS. These changes are not uniform and depend on multiple factors, such as dimensions of the lesion and the contribution of different nerve fibers, as well as immunological, genetic and environmental factors. Consequently, several different pathophysiological mechanisms have been identified—mainly from animal studies—that lead to the symptom of pain.<sup><a href="http://jneurology.wordpress.com/article/clinical-assessment-of-pain-23lvr9hhdbqmt-11/#B2">2</a></sup> From these studies, a mechanism-based classification of pain was suggested.<sup><a href="http://jneurology.wordpress.com/article/clinical-assessment-of-pain-23lvr9hhdbqmt-11/#B3">3</a></sup> Such classifications have implications for the development and application of treatment approaches, in terms of defining pharmacological targets and identifying patients who are likely to benefit from the various available therapies.<br />
To implement a mechanism-based classification of pain, such underlying pain-generating processes need to be reliably detected in patients. A thorough clinical investigation can reveal positive and negative symptoms and signs that potentially allow differentiation between subtypes of pain. Quantitative sensory testing (QST) is a precise way to identify somatosensory disturbances. The German Research Network on Neuropathic Pain, for example, has developed a standardized and comprehensive QST protocol, which consists of seven tests that measure 13 parameters of thermal and mechanical pain perception.<sup><a href="http://jneurology.wordpress.com/article/clinical-assessment-of-pain-23lvr9hhdbqmt-11/#B4">4</a></sup> QST data from more than 1,200 patients with neuropathic pain have so far been collected, and several relevant phenotypic subgroups can be described. Interestingly, these distinct subgroups occur across etiologies. This approach is currently reserved for research purposes or use in early phase II trials—QST is too time intensive and expensive to be used on a day-to-day basis in the clinic—so a need exists to develop alternative assessment tools that could be used in later phases of clinical trials and in routine clinical work.<br />
Scholz and colleagues<sup><a href="http://jneurology.wordpress.com/article/clinical-assessment-of-pain-23lvr9hhdbqmt-11/#B1">1</a></sup> have attempted to meet this need by developing a practical, standardized assessment of pain-related symptoms and signs to differentiate distinct pain phenotypes. The investigators prospectively assessed the symptoms and signs of 130 patients with peripheral neuropathic pain—caused by diabetic polyneuropathy, postherpetic neuralgia or radicular low back pain—and 57 patients with non-neuropathic low back pain, by means of a structured interview and a standardized bedside examination. The interview consisted of 16 questions that explored pain localization, evoked pains, pain quality and further sensory qualities, such as dysesthesia and numbness. The physical examination included 23 bedside tests that provided information about trophic and autonomic signs, evoked pains and sensory deficits. From the results of the interview and bedside examination, Scholz and colleagues were able to determine six subgroups of patients with neuropathic pain and two subgroups of patients with non-neuropathic pain.<br />
The physical examination was essential for the distinction of pain subtypes, with the response to pinprick being the most sensitive and most specific single test for distinguishing between neuropathic and non-neuropathic pain. Among patients with neuropathic pain, a positive result in the straight-leg-raising test was highly specific for radicular low back pain, whereas a decreased response to vibration was very sensitive and specific for detecting diabetic neuropathy and distinguishing this condition from postherpetic neuralgia. The responses to cold temperature and trophic changes were also essential for identifying pain subtypes. From their initial analysis to find out the best discriminatory procedures for identifying pain subtypes, Scholz and colleagues proposed an assessment tool comprising six interview questions and ten physical tests, which they named ‘Standardized Evaluation of Pain’ (StEP).<br />
In the second part of the study, StEP was applied to an independent group of 137 patients with chronic low back pain for validation. For each patient, a diagnosis of neuropathic or non-neuropathic (axial) low back pain was made by an interdisciplinary team of clinical experts. Another group of investigators, who were blind to the diagnoses, applied StEP to the patients. Through use of this assessment, the investigators were able to identify patients with radicular pain with 92% sensitivity and 97% specificity. This was superior to the Douleur Neuropathique en 4 Questions—an established screening tool for neuropathic pain that consists of seven interview questions and three physical tests<sup><a href="http://jneurology.wordpress.com/article/clinical-assessment-of-pain-23lvr9hhdbqmt-11/#B5">5</a></sup>—which was applied in parallel to StEP.<br />
On the basis of the data reported by Scholz et al., we conclude that StEP will have an important role in future multicenter treatment trials. Until now, inclusion criteria for studies investigating new analgesic agents have relied almost exclusively on the nature of the underlying disease. Furthermore, study end points designed to determine treatment efficacy have relied mainly on overall pain intensity. With StEP, a validated bedside test is available whereby neuropathic pain can be distinguished from non-neuropathic pain, and information can also be gained to identify subtypes of pain, independently from disease etiology. This assessment technique should enable much more sophisticated study designs and data analyses, by identifying subgroups of patients with pain that can be correlated with their response to analgesic treatment. Such improvements should also lead to a better understanding of underlying pain mechanisms and drug action.<br />
StEP could also be a useful supplementary technique for diagnosing pain in the clinic. Differentiating between neuropathic and non-neuropathic pain can be clinically challenging, and is of the utmost importance, because the two conditions require different treatment strategies. As with other screening tools, such as the patient-oriented questionnaire painDETECT<sup><a href="http://jneurology.wordpress.com/article/clinical-assessment-of-pain-23lvr9hhdbqmt-11/#B6">6</a></sup>—which has both a sensitivity and specificity of 80% for detecting neuropathic pain components in patients with low back pain—StEP cannot and is not meant to replace a thorough clinical examination of patients with pain. As stated by Scholz et al.,<sup><a href="http://jneurology.wordpress.com/article/clinical-assessment-of-pain-23lvr9hhdbqmt-11/#B1">1</a></sup> further studies are needed to determine the accuracy of StEP in distinguishing neuropathic pain from non-neuropathic pain in conditions other than low back pain.<br />
In conclusion, the study from Scholz and colleagues<sup><a href="http://jneurology.wordpress.com/article/clinical-assessment-of-pain-23lvr9hhdbqmt-11/#B1">1</a></sup> demonstrated a very promising bedside tool for pain assessment that differentiates pain phenotypes independently from disease etiology. The validation of this assessment for low back pain strongly supports the concept of a mechanism-based classification of pain and is a move towards developing better targeted analgesic therapies.<br />
<br />
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Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com1tag:blogger.com,1999:blog-115799600153427562.post-39495427783363743032011-12-28T10:24:00.000-08:002012-12-06T01:04:50.458-08:00Bilateral facial nerve palsy<div style="background-color: white; color: black;">
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Foix-Chavany-Marie (bi-opercular) syndromeIn 1926, Foix, Chavany, and Marie described an acquired syndrome of faciopharyngoglossomasticatory diplegia, caused by bilateral infarction of the anterior operculum (eg, anterior choroidal artery infarction). Clinical features included: facial diplegia, dysarthria, pseudobulbar palsy, cognitive deficits, and seizures. Foix-Chavany-Marie syndrome is also known as the biopercular syndrome (descriptively based on the typical associated lesions affecting the anterior operculum bilaterally) or faciopharyngoglossomasticatory diplegia with automatic voluntary association (descriptively based on the clinical features). Essentially this is a cortico-subcortical type of suprabulbar palsy.</span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;"></span><br />
<a name='more'></a><span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;"><br /></span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Clinically there is loss of voluntary movements of the jaw, face, pharynx, and tongue, with preserved automatic and reflex movements. For example, there may be a prominent severe facial diplegia to volitional actions (affecting both the upper and lower face, so-called "pseudoperipheral" facial palsy), with impaired volitional eye closure, inability to close the jaw, dysphagia, anarthria, and inability to protrude the tongue. However, corneal reflexes, jaw jerk, and swallowing reflexes are preserved (although the gag reflex is typically diminished or absent). Also preserved are "automatic" movements, including jaw opening with yawning, blinking (spontaneous or to threat), emotional smile, facial muscle contraction during crying, ability to contract the frontalis muscle with upgaze, and ability to close the eyes during sleep. Other possible neurologic manifestations include distal weakness in the arms, cheiro-oral paresthesias, and Broca aphasia.</span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Most cases are caused by ischemic strokes, but postsurgical, infectious (eg, Herpes simplex encephalitis, HIV, cerebral toxoplasmosis, etc.), epileptic (typically reversible in childhood epilepsy syndromes), traumatic, developmental (eg, bilateral perisylvian dysgenesis resulting from neuronal migration disorders), and rarely neurodegenerative causes are also recognized. Foix-Chavany-Marie syndrome may be confused with conditions causing bilateral peripheral facial dysfunction (eg, botulism, Guillain-Barré syndrome, or myasthenia).</span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Heerdfordt syndrome (neurosarcoidosis)Heerdfordt syndrome is a variety of neurosarcoidosis.</span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Manifestations include:• fever• uveitis• parotid gland swelling (unilateral or bilateral)• facial paresis (unilateral or bilateral)</span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Localization of the lesions responsible for facial paresis has been controversial. Proposed localizations have included (1) direct facial nerve compression by swollen parotid glands; (2) lesions within the facial canal (based on accompanying taste disturbance in some cases); and (3) lesions of the cerebellopontine angle that spread distally into the facial canal (based on electrical and mechanical stimulation studies and MRI). Treatment with immunosuppressive therapy can relieve symptoms, including facial paresis. Enhancing lesions on MRI may resolve with corticosteroid therapy.</span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Lyme neuroborreliosisFacial palsy is common in patients with Lyme neuroborreliosis and may occur in up to half of patients with Borrelia burgdorgeri meningopolyradiculoneuritis. It is particularly common in children with Lyme neuroborreliosis. Cases with a unilateral facial palsy and a history of tick bite and/or erythema chronicum migrans in the head/neck region generally have the facial palsy on the same side as the bite, suggesting direct nerve invasion by Borrelia burgdorferi in most unilateral cases. Whether this is also true in bilateral cases is not clear. Facial palsy generally occurs in the setting of meningitis and is often bilateral (about one third of cases with facial paresis due to Lyme disease). Approximately one third of cases are initially complete.</span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Manifestations can include:• fever• headache• facial paresis (unilateral or bilateral)• CSF pleocytosis and increased protein• MRI enhancement of tentorium and the trigeminal and facial nerves</span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Oral doxycycline is an effective and convenient therapy for Lyme-disease associated facial paresis. With therapy, 90% recover without sequelae within 6 months. Recovery is probably lower with bilateral facial paresis, but still approximately two thirds recover.</span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Melkersson-Rosenthal syndrome (OMIM #155900)Melkersson-Rosenthal syndrome (OMIM #155900) is a triad of (1) recurrent facial paresis (unilateral or bilateral); (2) relapsing facial edema, involving especially the lips; and (3) associated fissured tongue (lingua plicata or "scrotal tongue"). The complete triad is present, though, in less than one third of patients. Onset is often in childhood. Residual facial paresis generally increases with each episode and with concomitant development of progressive synkinesias. The gene locus is on 9p11.</span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Möbius syndrome (OMIM #157900)Möbius syndrome (OMIM #157900) is a syndrome of rhombencephalic maldevelopment involving predominantly brainstem motor nuclei and axons, as well as traversing long tracts. Vascular insufficiency prior to the 6th week of gestation involving the proximal sixth intersegmental artery may be responsible. Most cases are sporadic but inherited forms have been linked to 13q12.2-q13, 3q21-q22, and 10q21.3-q22.1.</span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">The syndromic definition varies somewhat across authors. Some label all cases of congential facial paresis as Möbius syndrome, whereas others restrict it to cases of congenital sixth and seventh nerve paresis with skeletal defects.</span><br />
<span style="display: inline ! important; float: none; font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;">Manifestations may include:• facial diparesis• bilateral (or rarely unilateral) ocular abduction paresis• Duane retraction syndrome• congenital fibrosis of ocular muscles• orofacial malformations (eg, cleft palate/cleft lip, microglossia, micrognathia)• paresis of lower cranial nerves (IX-XII), especially XII• absence of pectoralis major muscle (Poland anomaly)• terminal transverse limb defects• diaphragmatic anomalies• poor motor development• poor coordination• feeding difficulties in infancy• drooling• respiratory abnormalities.</span><br />
<br style="font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: normal; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;" />
<b style="font-family: 'Trebuchet MS',Trebuchet,Verdana,sans-serif; font-size: 13px; font-style: normal; font-variant: normal; font-weight: bold; letter-spacing: normal; line-height: normal; orphans: 2; text-indent: 0px; text-transform: none; white-space: normal; widows: 2; word-spacing: 0px;"><span style="font-size: 11px;">References:</span></b><br />
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Asenbauer B, McEntagart M, King MD, Gallagher P, Burke M, Farrell MA. Chronic active destructive herpes simplex encephalitis with recovery of viral DNA 12 years after disease onset. Neuropediatrics 1998;29:120-3.<br />
Becker PS. Developmental Foix-Chavany-Marie syndrome: polymicrogyria or macrogyria? Ann Neurol 1990;27:693-4.<br />
Becker PS, Dixon AM, Troncoso JC. Bilateral opercular polymicrogyria. Ann Neurol 1989;25:90-2.<br />
Biller J, Asconape J, Challa VR, Toole JF, McLean WT. A case for cerebral thromboangiitis obliterans. Stroke 1981;12:686-9.<br />
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Cellerini M, Mascalchi M, Salvi F, Muscas GC, Dal Pozzo G. MRI of congenital Foix-Chavany-Marie syndrome. Pediatr Radiol 1995;25:316-7.<br />
Christen HJ, Hanefeld F, Kruse E, Imhauser S, Ernst JP, Finkenstaedt M. Foix-Chavany-Marie (anterior operculum) syndrome in childhood: a reappraisal ofWorster-Drought syndrome. Dev Med Child Neurol 2000;42:122-32.<br />
Colamaria V, Sgro V, Caraballo R, et al. Status epilepticus in benign rolandic epilepsy manifesting as anterior operculum syndrome. Epilepsia 1991;32:329-34.<br />
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Foix C, Chavany JA. Diplégie faciales (facio-linguo-pharingo-masticatrices), d'origine corticale, avec quelques considerations sur les paralysies pseudo-bulbaires et la localization des centres corticaux de l'estrémité céphalique. Ann Med 1926;20:480-98.<br />
Foix C, Chavany JA, Marie J. Diplégie facio-linguo-masticatrice d'origine cortico-suous-cortical sans paralysie des members. Rev Neurol 1926;33:214-9.<br />
Graff-Radford NR, Bosch EP, Stears JC, Tranel D. Developmental Foix-Chavany-Marie syndrome in identical twins. Ann Neurol 1986;20:632-5.<br />
Grattan-Smith PJ, Hopkins IJ, Shield LK, Boldt DW. Acute pseudobulbar palsy due to bilateral focal cortical damage: the opercular syndrome of Foix-Chavany-Marie. J Child Neurol 1989;4:131-6.<br />
Gropman AL, Barkovich AJ, Vezina LG, Conry JA, Dubovsky EC, Packer RJ. Pediatric congenital bilateral perisylvian syndrome: clinical and MRI features in 12 patients. Neuropediatrics 1997;28:198-203.<br />
Hevner RF, Horoupian DS. Pena-Shokeir phenotype associated with bilateral opercular polymicrogyria. Pediatr Neurol 1996;15:348-51.<br />
Iannetti P, Raucci U, Basile LA, et al. Benign epilepsy of childhood with centrotemporal spikes and unilateral developmental opercular dysplasia. Childs Nerv Syst 1994;10:264-9.<br />
Grassi MP, Borella M, Clerici F, Perin C, Bini MT, Mangoni A. Reversible bilateral opercular syndrome secondary to AIDS-associated cerebral toxoplasmosis. Ital J Neurol Sci 1994;15:115-7.<br />
Lang C, Reichwein J, Iro H, Treig T. Foix-Chavany-Marie-syndrome--neurological, neuropsychological, CT, MRI, and SPECT findings in a case progressive for more than 10 years. Eur Arch Psychiatry Neurol Sci 1989;239:188-93.<br />
Mariani C, Spinnler H, Sterzi R, Vallar G. Bilateral perisylvian softenings: bilateral anterior opercular syndrome (Foix-Chavany-Marie syndrome). J Neurol 1980;223:269-84.<br />
Mateos V, Salas-Puig J, Campos DM, Carrero V, Andermann F. Acquired bilateral opercular lesions or Foix-Chavany-Marie syndrome and eating epilepsy. J Neurol Neurosurg Psychiatry 1995;59:559-60.<br />
Nisipeanu P, Rieder I, Blumen S, Korczyn AD. Pure congenital Foix-Chavany-Marie syndrome. Dev Med Child Neurol 1997;39:696-8.<br />
Redondo L, Mir J, Perez de Leon JA, et al. HIV related Foix-Chavany-Marie syndrome. Neurologia 2003;18:741-5.<br />
Sasaguri H, Sodeyama N, Maejima Y, Kanda T, Mizusawa H. Slowly progressive Foix-Chavany-Marie syndrome associated with chronic herpes simplex encephalitis. J Neurol Neurosurg Psychiatry 2002;73:203-4.<br />
Shevell MI, Carmant L, Meagher-Villemure K. Developmental bilateral perisylvian dysplasia. Pediatr Neurol 1992;8:299-302.<br />
Szabo K, Gass A, Rossmanith C, Hirsch JG, Hennerici MG. Diffusion- and perfusion-weighted MRI demonstrates synergistic lesions in acute ischemic Foix-Chavany-Marie syndrome. J Neurol 2002;249:1735-7. Erratum in: J Neurol 2003;250:380.<br />
Villa G, Caltagirone C. Speech suppression without aphasia after bilateral perisylvian softenings (bilateral rolandic operculum damage). Ital J Neurol Sci 1984;5:77-83.<br />
Weller M. Anterior opercular cortex lesions cause dissociated lower cranial nerve palsies and anarthria but no aphasia: Foix-Chavany-Marie syndrome and "automatic voluntary dissociation" revisited. J Neurol 1993;240:199-208.<br />
Weller M, Poremba M, Dichgans J. Opercular syndrome without opercular lesions: Foix-Chavany-Marie syndrome in progressive supranuclear motor system degeneration. Eur Arch Psychiatry Neurol Sci 1990;239:370-2.<br />
Guillain-Barre syndrome:Ropper AH. Further regional variants of acute immune polyneuropathy. Bifacial weakness or sixth nerve paresis with paresthesias, lumbar polyradiculopathy, and ataxia with pharyngeal-cervical-brachial weakness. Arch Neurol 1994;51:671-5.<br />
Leukemia/lymphoma/carcinomatous meningitis:Ozcakar L, Akinci A, Ozgocmen S, Aksu S, Cetin E. Bell's palsy as an early manifestation of acute lymphoblastic leukemia. Ann Hematol 2003;82:124-6.<br />
Sasaki MG, Leite PG, Leite AG, de Almeida SM. Bilateral peripheral facial palsy secondary to lymphoma in a patient with HIV/AIDS: a case report and literature review. Braz J Infect Dis 2002;6:50-4.<br />
Schattner A, Kozack N, Sandler A, Shtalrid M. Facial diplegia as the presenting manifestation of acute lymphoblastic leukemia. Mt Sinai J Med 2001;68:406-9.<br />
Lyme disease:Angerer M, Pfadenhauer K, Stohr M. Prognosis of facial palsy in Borrelia burgdorferi meningopolyradiculoneuritis. J Neurol 1993;240:319-21.<br />
Christen HJ, Bartlau N, Hanefeld F, Eiffert H, Thomssen R. Peripheral facial palsy in childhood--Lyme borreliosis to be suspected unless proven otherwise. Acta Paediatr Scand 1990;79:1219-24.<br />
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Siwula JM, Mathieu G. Acute onset of facial nerve palsy associated with Lyme disease in a 6 year-old child. Pediatr Dent 2002;24:572-4.<br />
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James DG. Differential diagnosis of facial nerve palsy. Sarcoidosis Vasc Diffuse Lung Dis 1997;14:115-20.<br />
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Vasculitis:Nikolaou AC, Vlachtsis KC, Daniilidis MA, Petridis DG, Daniilidis IC. Wegener's granulomatosis presenting with bilateral facial nerve palsy. Eur Arch Otorhinolaryngol 2001;258:198-202.<br />
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Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com1tag:blogger.com,1999:blog-115799600153427562.post-36353426727930797012011-12-27T09:18:00.001-08:002012-12-06T01:21:00.434-08:00Visually-evoked rootingThe group of reflexes collectively known as "primitive reflexes", reviewed by Schott and Rossor,2 include the grasp, snout, palmomental, and rooting reflexes. They are usually associated with neurodegenerative diseases causing dementia and, as the authors point out, loosely linked to frontal lobe pathology, but their exact physiological and anatomical substrates are poorly understood.<br />
The well known tactile-evoked rooting reflex is the movement of both lips towards the examiner’s finger when stroking the lateral side of the upper lip. However, there has been very little written about the related phenomenon of visually-evoked rooting.<br />
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Visually-evoked rooting is an extreme form of primitive reflex which is very rarely seen by neurologists. Its real frequency is unknown, presumably because it is only present in advanced stages of dementia in institutionalised patients who are rarely comprehensively examined by a consultant neurologist or elderly care physician. It appears similar to the behaviour of ungulates when approached with an open hand containing food. It seems possible that visually-evoked rooting is different from the more classical tactile rooting reflex which is seen in normal human infants from about 28 weeks in utero until 16 weeks post term.3 Although visual rooting has been reported in childhood autism,4 it is not present in normal young adults.5 Visually-evoked rooting may be more akin to the Babinski sign which van Gijn and others have viewed as a phylogenetically primitive type of flexor synergy withdrawal response of the leg.6,7<br />
Visually-evoked rooting is an extreme form of primitive reflex which is very rarely seen by neurologists<br />
We suspect this extraordinary physical sign is as unfamiliar to most neurologists and elderly care physicians as it was to ourselves.<br />
<br />
REFERENCES<br />
Perkin GD. Some neurological signs. J Neurol Neurosurg Psychiatry 2002;73:110.[Free Full Text]<br />
Schott JM, and Rossor MN. The grasp and other primitive reflexes. J Neurol Neurosurg Psychiatry 2003;74:558–60.[Abstract/Free Full Text]<br />
Sheppard JJ, Mysak ED. Ontogeny of infantile oral reflexes and emerging chewing. Child Dev 1984;55:831–43.[Medline]<br />
Minderaa RB, Volkmar FR, Hansen CR, et al. Snout and visual rooting reflexes in infantile autism. J Autism Dev Disord 1985;15:409–16.[Medline]<br />
Brown DL, Smith TL, Knepper LE. Evaluation of five primitive reflexes in 240 young adults. Neurology 1998;51:322.[Free Full Text]<br />
van Gijn J. The Babinski sign: the first hundred years. J Neurol 1996;243:675–83.[Medline]<br />
Marie P, and Foix Ch. Réflexes d’automatisme médullaire et réflexes dits "de défense": le phénomène des raccourcisseurs. Semaine médicale 1913;33:505–8.Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com1tag:blogger.com,1999:blog-115799600153427562.post-23266789728308320722011-12-27T09:17:00.001-08:002012-12-06T01:09:51.408-08:00Examine eye movementsAs with all aspects of the neurological examination, important clues come from a thorough and appropriate history. In relation to eye movement disorders the patients may be complaining of double vision, in which case they should be asked whether it is constant or intermittent; does it occur, or is it maximal, in certain directions of gaze; what is the relationship of one image with the other; and have they tried covering one eye and did that relieve the symptom? A less frequently reported symptom is oscillopsia, an illusion of movement of stationary objects, when enquiries need to be made whether the movement is horizontal or vertical, and does it become maximally apparent in certain positions of gaze, as for example in downbeat nystagmus when the oscillopsia is maximal on down gaze.<br />
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The first part of any examination is observation and again this may provide clues to the diagnosis. Look out for abnormal head postures, turns or tilts, the latter typically occurring in an isolated trochlear nerve palsy; abnormal patterns of eye–head coordination, such as the head thrusts seen in ocular motor apraxia; abnormalities of the eyelids such as ptosis in an oculomotor palsy and myasthenia gravis, or retraction as is seen in thyroid ophthalmopathy and progressive supranuclear palsy.<br />
<br />
STATIC EYE MOVEMENTS<br />
We are now ready to examine the eye movements, hopefully with the benefit of some clues to the diagnosis already obtained from the history and simple observation of the patient.<br />
Ocular misalignmentFirst ask the patient to look at a distant object and observe any obvious ocular misalignment or abnormal, spontaneous eye movements. If one eye is deviated inward relative to the other this is referred to as an esotropia, whereas if there is an outward deviation this is called an exotropia. If there is a vertical misalignment it is described in relation to the laterality of the higher eye (for example, a right hypertropia indicates that the right eye is higher than the left).<br />
Monocular or binocular diplopia?If the patient is complaining of diplopia it is essential to next differentiate a disparity in retinal stimulation between the two eyes (binocular diplopia), from the rarer form of diplopia which is present in one eye only (monocular diplopia). This is simply done by covering one eye and then the other to see if the diplopia disappears or persists in one eye only. Monocular diplopia occurs, with few exceptions, when there are abnormalities of the ocular refractive surfaces and media, producing multiple overlapping images on the retina. It is usually abolished or improved by getting the patient to observe a target through a pinhole. The commonest cause is myopic astigmatism, but monocular diplopia may occur with early cataracts, especially under conditions of dim illumination. Other causes include abnormalities of the cornea and iris, foreign bodies in the aqueous or vitreous humour, and retinal disease. Rarely, when monocular diplopia occurs in both eyes after each is covered in turn, it may be due to occipital cortex pathology, or there can be multiple images (cerebral polyopia). If the monocular diplopia does not disappear or improve with a pinhole it is either due to one of the ocular refractive problems described above, or it is psychogenic in origin, the cerebral causes being exceedingly rare.<br />
If we take the commonest clinical scenario of binocular diplopia, a systematic approach to evaluation is required. As well as determining the nature of the separation of the two images and the direction of maximal separation, enquiries about any family history of strabismus (squint), or a childhood history of orthoptic treatment should be made.<br />
We next need to find out which muscle is weak. To do this the range and speed of movement of the two eyes are examined, first with ductions (one eye viewing) and then with versions (both eyes viewing) in the nine cardinal positions of gaze (up and left, up, up and right, left, straight ahead (primary position), right, down left, down, down right). Any limitation of ocular movement when examining ductions is recorded as a percentage of the normal range and if there are any differences on versions these are noted.<br />
If the eyes are clearly misaligned at rest or on movement it should be ascertained at an early stage if one is dealing with a non-comitant or comitant strabismus; the degree of misalignment varies with gaze position in the first, but not in the second:<br />
Non-comitance suggests a recent paretic or restrictive aetiology (occurring when an ocular muscle is unable to move the globe because its antagonistic muscle fails to relax—for example in thyroid ophthalmopathy, when the inferior rectus may become fibrosed and restricts upward gaze).<br />
Comitance is characteristic of childhood strabismus, and diplopia in such circumstances is usually due to decompensation of a long-standing phoria (a deviation of the visual axes which occurs only when binocularity is interrupted), normally kept in check by fusional mechanisms (a latent deviation). This may sometimes be observed after relatively minor head trauma.<br />
The term tropia refers to a deviation of the visual axes when both eyes are viewing, which is not kept in check by fusion and is present at all times (a manifest deviation).<br />
To sort out these aspects of ocular misalignment the cover/uncover and alternate cover tests are used:<br />
In the cover/uncover test, used to detect tropias, the patient, wearing appropriate refractive correction, is asked to fixate a distant target (for example, a letter on the Snellen chart) with the eyes in the primary position (fig 1). One eye is covered and any immediate movement of the uncovered eye is observed. Cover tests rely on the fact that foveation occurs in an eye that is forced to fixate; if the retinal image was not directed on to the fovea before the eye took up fixation, what is known as a movement of redress will be noted as the uncovered eye now fixates the target. This gives an indication of the degree of misalignment of the visual axes when binocular viewing took place. If the uncovered eye moves to take up fixation a manifest deviation is present (a tropia). Inward movement of the uncovered eye indicates an exotropia (the eye had previously been outwardly deviated), and an outward movement an esotropia (the eye had previously been inwardly deviated). A vertical deviation may be either a hypotropia or a hypertropia, depending on whether the eye moves up or down, respectively. It should be noted that the convention is that if there is a vertical deviation of the eyes, the higher of the two is referred to as hypertropic/hyperphoric, regardless of which eye is at fault.<br />
<br />
<br />
<br />
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<br />
Figure 1 (A) The cover/uncover test, showing an<br />
esophoria. Grey bars indicate the position of the eye when under cover. (i) At<br />
rest the visual axes are aligned correctly. (ii) When the cover is placed before<br />
the left eye, the eye no longer fixates and moves inwards. (iii) On removal of<br />
the cover the eye moves outwards to take up fixation, indicating an esophoria.<br />
(B) The alternate cover test, showing an esotropia. (i) At rest, with both eyes<br />
viewing, there is a manifest inward deviation of the left eye. (ii) A cover<br />
placed before the non-fixating left eye causes no movement. (iii) When the right<br />
eye is occluded, the left eye is forced to fixate, and a movement of redress<br />
occurs (primary deviation). The resulting additional innervation to the<br />
contralateral muscle leads to deviation of the sound eye under the cover (the<br />
secondary deviation). Note that the secondary deviation is greater than the<br />
primary deviation. (iv) When the cover is transferred to the left eye both eyes<br />
assume their original position.<br />
<br />
<br />
<br />
If a tropia is present the examiner should next determine whether it is comitant or non-comitant by seeing if the magnitude of the deviation varies with the position of the eye.<br />
If no tropia is present in the uncovered eye then the examiner’s attention moves to the covered eye. As the occluder is removed the eye is observed to determine whether it has moved to assume fixation just after it was uncovered, referred to as a latent deviation (a heterophoria). Depending on the direction of the deviation this may be classified as an exophoria, esophoria, hypophoria or a hyperphoria. The test is then repeated, and the same observations made while covering the other eye.<br />
The alternate cover test is more dissociating than the cover/uncover test (because there is no possibility for binocular fusion which it effectively breaks) to show the maximal deviation—any tropia plus any latent phoria. While the patient fixates a target the occluder is quickly switched from eye to eye to prevent binocular viewing, allowing sufficient time for the eyes to settle in their new position after each transfer. The test should be performed in the nine cardinal positions of gaze to determine the direction of gaze that elicits the maximal shift of eye position on switching the occluder. While ensuring that the patient is never allowed to regain fixation during transfer of the occluder, the examiner notes the movement of the newly uncovered eye as the occluder is transferred from one eye to the other. Movement of the uncovered eye may indicate either a heterotropia or a heterophoria, but the alternate cover test will not differentiate between the two. The cover/uncover test should therefore be performed before the cover/uncover test, to determine if a tropia is present.<br />
Having completed the cover tests, further examination of versions to determine the paretic muscle is best achieved using a bright pen torch with a red glass or piece of perspex (obtained from a pair of red-green glasses found in many toy shops!) placed in front of the right eye. The patient now sees a white and a red image if there is displacement of the images and can describe their location in relation to each other:<br />
If the displacement is horizontal in the primary position then the position generating the maximum separation is next identified. With the knowledge that the outer of the two images derives from the paretic muscle and only the lateral rectus and medial rectus muscles are involved in horizontal movements, the paretic muscle can be determined.<br />
If the patient complains of vertical or oblique diplopia ascertain whether the red image is higher or lower. The hypertropic eye always produces the lower image. Therefore, if the patient has a left hypertropia the involved muscles are either the elevators of the right eye (superior rectus and inferior oblique muscles), or the depressors of the left eye (inferior rectus and superior oblique muscles) and conversely for right hypertropia. The number of possibilities can be further reduced by ascertaining whether the misalignment is greater on right or left gaze—the recti muscles being responsible for vertical movements in the abducted position, and the obliques in the adducted position of gaze. Finally, determining which of these two muscles is paretic is decided by finding whether the deviation is maximal in up or down gaze.<br />
If the patient complains of an oblique vertical separation of images then a simple test for weakness of the superior oblique muscle, as in a trochlear nerve palsy, is to hold a pencil or ruler horizontally in front of the patient and ask him or her to look at the middle of the object as it is slowly lowered. If the patient experiences vertical separation of the images, which are oblique to one another forming a V shape, the point of the V is directed towards the side of the weakened superior oblique muscle.<br />
In some instances when performing these tests there may be no differential vertical deviation; this situation occurs with chronic palsies due to an adaptive phenomenon, termed "spread of comitance". To work out which vertical muscle is paretic the Bielschowsky head tilt test is performed; the vertical deviation is compared with the alternate cover test in right and left head tilt positions (fig 2). The degree of misalignment will increase when the head is tilted to the side of the paretic muscle if the ipsilateral intorters (superior oblique and superior rectus) are weak, and to the opposite side if the extorting muscles (inferior oblique and inferior rectus) are weak. In practice an increased misalignment on head tilt is usually indicative of an ipsilateral superior oblique palsy. The test is less often positive with palsies of the vertical recti or inferior oblique muscles. The explanation for the effect lies in the fact that a head tilt to either shoulder induces an ocular counter-rolling, which is mediated by the ipsilateral intorters (superior rectus and superior oblique) and the contralateral extorters (inferior rectus and inferior oblique). If, for example, the ipsilateral superior oblique is paretic, the superior rectus on the same side receives excessive innervation to intort the eye, and by virtue of its relatively unopposed primary action elevates the eye.<br />
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Figure 2 The Bielschowsky test for vertical diplopia, illustrated for a right<br />
fourth (trochlear) nerve palsy. See text for full explanation.<br />
If more than one extraocular muscle is paretic it may be difficult to determine which one is involved and a more sophisticated test may be required such as a Hess chart, usually performed by an orthoptist.<br />
<br />
DYNAMIC EYE MOVEMENTS<br />
We now turn to assessing the more dynamic aspects of ocular motility. First, however, ask the patient to fixate on a stationary target and look for nystagmus or extraneous saccades such as square wave jerks.<br />
SaccadesNext assess the patient’s ability to perform voluntary saccades by asking him or her to look to the left and right, and up and down. Disturbances in the initiation of saccades may lead to a prolonged latency, or the addition of a head movement or blink to initiate the saccade, the latter in congenital or acquired oculomotor apraxia, and various degenerative conditions such as Huntington’s disease. It should also be possible to gauge the normality of the saccadic velocity.<br />
Then instruct the patient to rapidly look at a suddenly appearing object, for example a rapidly lifted finger when placing your hands on either side of, and 40–50 cm away from, the patient’s face. This tests for reflexive saccades and in addition to assessing the saccadic latency and velocity the saccadic accuracy can now be evaluated—saccadic overshoot (hypermetria) or undershoot (hypometria).<br />
While assessing saccadic function also look out for evidence of a partial internuclear ophthalmoplegia in which there is slowed adduction on the side of a lesion of the medial longitudinal fasciculus, with abducting nystagmus in the other eye. Sometimes this may be difficult to pick up so get the patient to make saccades between obliquely placed targets. Because the velocity is slowed in the horizontal and not the vertical plane, the resulting saccade is L shaped.<br />
Predictive saccades are tested by alternately raising a finger of one hand and then the other in a predictable and regular pattern. The patient is asked to make saccades back and forth to the moving finger. Normally after a few saccades they anticipate the appearance of the stimulus and make a saccade in advance. Abnormalities are observed in neurodegenerative disorders such as Parkinson’s disease.<br />
Any slowing of saccades can be accentuated by using an optokinetic striped drum, or measuring tape, when the repositioning saccades will appear clearly slowed.<br />
Smooth pursuitSmooth pursuit can be tested by asking the patient to track a small moving target, such as the head of a hat pin, at a distance of about 1 metre, while keeping their head stationary. Both horizontal and vertical smooth pursuit should be assessed. The target should be moved initially at a slow uniform speed and the pursuit eye movements observed to determine whether they are smooth, or broken up by catch-up saccades. This is a non-specific sign when present in both directions—for example, it may be due to ageing or cerebellar disease—or it may indicate a focal posterior cortical lesion if only present in one direction, in which case the abnormal pursuit is in the direction of the lesion. The speed should be gradually increased, but at high velocities (>50 degrees per second) all smooth pursuit eye movements will be broken up by saccades even in normal people.<br />
Despite their relevance for locomotion and social interaction in everyday situations, little is known about the cortical control of vertical saccades in humans. Results from mi-crostimulation studies indicate that both frontal eye fields (FEF) contribute to these eye movements. Patients with a damaged right FEF, who hardly made ver-tical saccades during visual exploration. This finding suggests that for the cortical control of exploratory vertical saccades, integrity of both FEF is indeed important.<br />
<br />
PRACTICE POINTS<br />
Eye movements should be examined in two stages, first when the eyes are static in different positions of gaze, and then dynamically.<br />
Static eye movement examination, particularly when the patient complains of diplopia, requires the correct use and interpretation of the cover/uncover and the alternate cover tests.<br />
Testing of dynamic eye movements involves examination of rapid conjugate eye movements, saccades, and smooth pursuit both horizontally and vertically.<br />
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Further reading<br />
C Kennard. Normal and abnormal eye movements. In: Luxon L, ed. A textbook of audiological medicine: clinical aspects of hearing and balance. London: Martin Dunitz, 2003:781–96.<br />
Leigh RJ, Zee DS. The neurology of eye movements. Fourth edition. Oxford University Press, 2006.<br />
Shaunak S, O’Sullivan E, Kennard C. Eye movements. In: Hughes RAC, ed. Neurological investigations. London: BMJ Publishing Group, 1997:253–82.<br />
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Optokinetic nystagmus<br />
The optokinetic system is often tested as part of the clinical examination using the striped optokinetic drum or a measuring tape moved in front of the eyes. However, because these occupy a small area of the visual field they in fact test smooth pursuit and not the optokinetic system. A full field revolving striped drum is required to elicit true optokinetic nystagmus. Reduced optokinetic nystagmus occurs in visual disorders, in pursuit system disorders, and in disorders of fast phases (saccades).<br />
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Vestibular system<br />
If the vestibulo-ocular system is functioning, normally passive rotation of the patient’s head with the patient instructed to look straight ahead should result in a slow eye movement so that the eyes move in the opposite direction to that of the head movement. This is known as the doll’s head (oculocephalic) manoeuvre and should be performed both horizontally and vertically. This technique is not only valuable for assessing vestibular function (space does not allow a full coverage of its assessment), but in the current context for differentiating infranuclear and nuclear gaze palsies when the response is absent, from supranuclear gaze palsies in which a normal doll’s head response is present.<br />
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CONCLUSIONS <br />
Examination of eye movements can usually be completed fairly quickly but all types of eye movement should be evaluated because they have different anatomical bases and therefore can provide clues to the possible location of lesions.Carlos Vázquezhttp://www.blogger.com/profile/09266699098392968330noreply@blogger.com2