Dear NZBill,
Thank you for your question and my condolences on your injury. As
usual, any information provided is not a substitute for direct medical
examination or advice.
The symptoms you describe appear to be a combination of effects. For
example, the asymmetry of the face is likely due to either damage to
the left facial nerve (Cranial Nerve VII) somewhere along its pathway
or at it's nucleus, or damage the cerebral cortex or brainstem in the
area of the cerebello-pontine angle, which you mention. Here is a
list of problems that can result in facial asymmetry:
http://www.fpnotebook.com/NEU9.htm
Here is an article that describes some of the anatomy and functions of the nerves:
http://www.emedicine.com/ent/topic8.htm
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As you mention, autonomic dysreflexia is one possible explanation for
some of the symptoms you describe. Another, more rare explanation, is
Poufour du Petit syndrome, which involves hyperactivity of the
sympathetic cervical chain (a bundle of nerves that controls a portion
of the sympathetic autonomic system). Here is a case report on this
syndrome, although the full text of the article is not available
online:
Avellanal M. Fernandez-Quero L. Barrios JM. Sanchez P. Navia J.
Pourfour du Petit syndrome: a case following a traffic accident with
severe cranioencephalic trauma. [Case Reports. Journal Article]
Intensive Care Medicine. 22(10):1090-92, 1996 Oct.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8923075
Here is the abstract:
"Poufour du Petit syndrome is an extraordinarily unusual clinical
condition produced by hyperactivity of the sympathetic cervical chain
as a consequence of irritation of these nerves. It causes an
ipsilateral mydriasis [dilation of the pupil], which, in patients
suffering a head injury as in the case reported here, can confuse the
diagnosis and disconcert physicians."
Here is a second article:
Kara M, Dikmen E, Akarsu C, Birol A. Unilateral hyperhydrosis in
Pourfour du Petit syndrome. Eur J Cardiothorac Surg. 2004
Aug;26(2):456-8.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15296919
"Upper limp hyperhydrosis is an idiopathic disease with bilateral
involvement. However, Pourfour du Petit syndrome, the opposite of
Horner syndrome, may result in unilateral upper limb hyperhydrosis. It
occurs following hyperactivity of the sympathetic cervical chain as a
consequence of irritation secondary to trauma. We report herein two
cases with Pourfour du Petit syndrome showing unilateral upper limb
hyperhydrosis. The patients presented with right-sided mydriasis and
ipsilateral hemifacial hyperhydrosis. The onset of disease was
followed by a trauma in both patients. They underwent upper thoracic
sympathectomy with favorable outcome. A history of an antecedent
trauma in patients with unilateral upper limb hyperhydrosis and
anisocoria may imply a possible diagnosis of Pourfour du Petit
syndrome."
----------
This article on brain injury has some discussion of midbrain injury
(see also Tables I and II):
http://www.walthamusa.com/articles/PODELL.pdf
This case report from the Naval Hospital at Camp Pendleton discusses
some other possible ramifications of midbrain injury, including loss
of taste on one side of the tongue (hemiageusia) and difficulty
walking (ataxic hemiparesis):
Johnson TM. Ataxic hemiparesis and hemiageusia from an isolated
post-traumatic midbrain lesion. [Case Reports. Journal Article]
Neurology. 47(5):1348-9, 1996 Nov.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8909461
Here is an excerpt:
"Closed-head injury frequently involves the dorsolateral aspects of
the rostral brainstem. This area of the brain is uniquely vulnerable
to injury from rotationally induced sheer forces. Patients who suffer
such injuries usually have diffuse axonal injury to other areas of the
brain. This is a case report of a patient with an isolated midbrain
lesion secondary to a motor vehicle accident (MVA) who developed
ataxic hemiparesis and ipsilateral hemiageusia."
The patient was a 22-year-old right-handed white man who was in
excellent health until he was involved in an MVA 1 month before being
seen in the Neurology clinic. In the accident, he suffered a
closed-head injury with loss of consciousness, as well as a minor
injury to his right knee. Evaluation at another hospital included a
brain MRI done 15 days after the MVA that demonstrated a small left
frontal subacute subdural hematoma and a focal contusion of the
splenium of the corpus callosum. When the patient presented to the
Neurology Clinic, his chief complaints were that of clumsiness of his
left arm and leg and the complete loss of taste on the left side of
his tongue. He had no other medical problems and was taking no
medications. The neurologic examination revealed that cognition was
intact. There was some subtle dysarthria of speech. Cranial nerves I
through XII were intact except for an abnormality of taste on the left
side of the tongue. The patient described a subjective "funny" feeling
in that part of the tongue and objectively had no perception of the
taste of sweet, salty, bitter, or acidic items. Taste was normal on
the right side of the tongue. There were no fasciculations, atrophy,
or signs of trauma to the tongue.
Motor examination revealed 5/5 strength on the right side and 5-/5
strength on the left side with weakness in a pyramidal distribution.
Sensation was intact to all modalities everywhere except the left side
of the patient's tongue. Cerebellar examination revealed a marked
decrease in the ability to perform rapid alternating movement,
heel-to-shin maneuvers, and toe-tapping on the left side. Gait was
slightly wide based. Reflexes were 2/4 on the right side with a flexor
plantar response and 3/4 on the left side with an extensor plantar
response.
A review of the initial MRI revealed, in addition to the subdural
hematoma and the contusion of the corpus callosum, a 3 times 2-mm area
of increased signal on T2-weighted images in the left lateral
mesencephalon inferior to the red nucleus Figure 1. An MRI obtained 60
days after the MVA revealed that the subdural hematoma and the
contusion of the corpus callosum had completely resolved. There was an
area of decreased signal consistent with hemosiderin on T2-weighted
axial and coronal images that corresponded to the midbrain lesion
noted on the initial MRI. There were no other abnormalities on the
second MRI. The patient has made good recovery, although he still has
some mild to moderate left sided dysmetria."
As the above article notes, patients with injury to the midbrain
usually have diffuse axonal injury (a type of brain injury that is not
localized) in other portions of the brain, which may explain some of
your symptoms.
----------
The University of Miami has a site on autonomic dysreflexia here:
http://calder.med.miami.edu/pointis/automatic.html
The UK SpinalNet also has an article:
http://www.spinalnet.co.uk/EEndCom/GBCON/homepage.nsf/(VIEWDOCSBYID)/67150DFCD7EA398700256C47003EDA59?OpenDocument
The Christopher and Dana Reed Paralysis Center has an overview:
http://www.paralysis.org/Health/HealthList.cfm?c=10
A comprehensive overview (and possibly the article you found) is
available at eMedicine, written by Dr. Campagnolo at the Barrow
Neurological Institute, one of the top centers in the world for the
treatment of neurological disease:
http://www.emedicine.com/pmr/topic217.htm
This article also discusses some aspects of treatment, focusing on rehabilitation:
"Rehabilitation Program:
? Physical Therapy: Physical therapists who treat SCI patients
need to have a good understanding of AD and be familiar with the signs
and symptoms of this potentially life-threatening condition. When
completing physical therapy sessions, the therapist needs to monitor
the urinary catheter for any blockage or twisting. If the patient
becomes hypertensive during therapy, he/she should be placed in an
upright position immediately, rather than remain in a supine or
reclining position. The therapist needs to complete careful inspection
to identify the source of painful stimuli (eg, catheter, restrictive
clothing, leg bag straps, abdominal supports, orthoses).
A less common cause of AD during physical therapy sessions may
originate with muscle stretching, either from range of motion or
passive stretching. If the patient develops AD, the physical therapist
needs to treat it as a medical emergency and be familiar with
established protocols for medical management within his/her particular
setting. The individual therapy session then must be discontinued to
allow the patient to stabilize and recover.
? Occupational Therapy: Occupational therapy is another discipline
involved extensively in the rehabilitation of individuals with SCI.
The occupational therapist also must be familiar with the signs and
symptoms of AD and be able to respond quickly if the condition
develops during a therapy session. The occupational therapist performs
extensive training in the performance of activities of daily living
with patients who have sustained SCI. Activities of daily living
include proper bowel and bladder management, which can help prevent
the occurrence of AD. The occupational therapist may be involved in
establishing a regular bowel program and also may complete patient and
family/caregiver education on this aspect of care. Both the
occupational and physical therapists should educate the patient and
family members about AD and ensure that they are familiar with
prevention strategies, signs and symptoms, and proper management of
the condition.
? Speech Therapy: Generally, the treatment provided by the speech
therapist is not associated with any painful stimuli below the lesion
that may precipitate an AD response; however, as health care providers
involved in the care of individuals with SCI, the speech therapist
must be familiar with the manifestations of this potential
life-threatening complication.
? Recreational Therapy: Recreational therapists also are important
members of the rehabilitation team, as they help patients with SCI to
become involved in recreational and social activities. As members of
the SCI team, they also must be knowledgeable about AD and know how to
respond appropriately if the patient develops symptoms during a
recreational therapy session."
The Medication section of the above document describes possible
medical treatments for autonomic dysreflexia. These are primarily
symptomatic treatments, not intended to treat the primary condition.
A second eMedicine article discusses brain injuries:
http://www.emedicine.com/neuro/topic153.htm
This eMedicine article by Dr. Cory Toth at the University of Calgary
discusses autonomic neuropathy due to many different causes (not
limited to trauma):
http://www.emedicine.com/neuro/topic720.htm
----------
Another possibility for the article you came across is this 121 page
document from the Southwest School of Botanical Medicine. It mentions
many of the disorders you recall, however it discusses multiple
neurological disorders, many of which are unlikely to be related to
your symptoms:
http://www.swsbm.com/EclecticMed/Eclectic%20Medicine_Part_8.pdf
This article, aimed at nurses, discusses general brain and spinal cord
injuries and contains many good diagrams:
http://connection.lww.com/Products/timbyessentials/documents/Ch41.pdf
-----------
This article from the Travis Roy Foundation discusses some
preventative measures to take to prevent exacerbations of autonomic
dysreflexia. There is also a link to a PDF booklet at the bottom of
the page:
http://www.travisroyfoundation.org/pages/resources-AD.htm
An autonomic dysreflexia treatment algorithm can be found here:
http://www.paraquad-nsw.asn.au/uploads/files/1061791801125_0.5779169152456723.pdf
This article from Australia discusses AR, as well as treatment:
http://www.paraquad-nsw.asn.au/uploads/files/1061791801125_0.5779169152456723.pdf
Here is a brief letter describing treatment of AR:
http://www.cmaj.ca/cgi/content/full/170/8/1210
The letter above lists further references at the bottom, including a
free full-text article:
Blackmer J. Rehabilitation medicine: 1. Autonomic dysreflexia. CMAJ
2003;169(9):931-5.
http://www.cmaj.ca/cgi/reprint/169/9/931?ijkey=d3281e8a9e153438b7fd563bab0f50d232e3b613
----------
Multiple other articles are available online with this Google search:
"autonomic dysreflexia" treatment
://www.google.com/search?q=%22autonomic+dysreflexia%22+treatment&hl=en&lr=&safe=off&start=0&sa=N
----------
This article lists some of the physical findings that may be present:
"? A sudden significant rise in both systolic and diastolic blood
pressures, usually associated with bradycardia, can appear. The normal
systolic blood pressure for SCI above T6 is 90-110 mm Hg. Blood
pressure 20-40 mm Hg above the reference range for such patients may
be a sign of AD.
? Profuse sweating above the level of lesion, especially in the
face, neck, and shoulders, may be noted, but it rarely occurs below
the level of the lesion because of sympathetic cholinergic activity.
? Goose bumps above, or possibly below, the level of the lesion may be observed.
? Flushing of the skin above the level of the lesion, especially in
the face, neck, and shoulders, frequently is noted.
? The patient may report blurred vision.
? Spots may appear in the patient's visual fields.
? Nasal congestion is common.
? No symptoms may be observed, despite elevated blood pressure."
----------
Here is another source of possible findings with midbrain injury:
http://www.gpnotebook.co.uk/simplepage.cfm?ID=-1207566313&linkID=22571&cook=yes
"? lesions of the upper midbrain - weakness of conjugate deviation
upwards and ptosis
? lesions of the lower midbrain - weakness of conjugate deviation
downwards - often accompanied by ptosis and weakness of convergence
? pupils unequal and dilated
? reactions to light and to convergence-accommodation may be both
lost, or just the former may be absent
? nuclear ophthalmoplegia may be asymmetrical
? headache, papilloedema, vomiting from hydrocephalus
? nystagmus and ataxia may result from injury to cerebellar pathways
? compression of lateral lemniscus may cause unilateral or bilateral deafness
? tremors, tonic convulsions, loss of consciousness may occur"
Here is a brief overview of the structures found in the midbrain and
their functions:
http://www.geocities.com/HotSprings/3468/11-01.html#MidBrain
More detail can be found at the Wikipedia midbrain page:
http://en.wikipedia.org/wiki/Midbrain
Here is the midbrain page from the University of Idaho:
http://www.sci.uidaho.edu/med532/midbrain.htm
A page from the UMass Medical neuroanatomy course (more advanced):
http://courses.umassmed.edu/mbb1/2004/bcv/auto.cfm
----------
Injury to the carotid arteries in the neck can also result in some
unusual symptoms. Here is such a case report:
Bilello JF. Davis JW. Kaups KL. Parks SN. Localized autonomic
abnormality: another clinical marker of blunt cervical vascular
injury?. [Case Reports. Journal Article] Journal of Trauma-Injury
Infection & Critical Care. 50(1):124-5, 2001 Jan.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11231682
Here is an excerpt:
"A 34-year-old man was involved in a high-speed motorcycle crash. He
suffered a right tension pneumothorax treated at the scene with needle
thoracostomy. He reported loss of consciousness. In the emergency
department, he was both hemodynamically and neurologically normal.
Chest radiograph showed multiple bilateral rib fractures. Radiographic
cervical spine evaluation was normal. The patient had no pain or
tenderness of the neck or spine. He remained neurologically intact,
with a Glasgow Coma Scale score of 15. Noncontrast computed
tomographic scan of the head was negative.
On hospital day 2, the patient complained of numbness of the left
hand. On physical examination, he was noted to have a marked,
localized coolness of the left arm between the elbow and wrist and of
the left leg between the knee and ankle, despite having a normal pulse
and capillary refill in each. There was decreased sensation and motor
strength in the left upper and lower extremities. His pupils were
equal and reactive to light.
Magnetic resonance imaging (MRI) of the head and spine was planned.
The patient subsequently developed acute respiratory distress and left
hemiplegia, which progressed to quadriplegia and unresponsiveness. He
was endotracheally intubated. A repeat computed tomographic scan of
the head without intravenous contrast was again negative. MRI of the
head and neck and four-vessel cervical angiogram were obtained. MRI
showed right cerebellar and lateral medullary infarcts. Angiography
showed complete right vertebral artery occlusion.
The patient was stabilized in the intensive care unit. He remained
quadriplegic and eventually was transferred to a rehabilitation
facility."
----------
Trauma to a nerve can also eventually result in reflex sympathetic
dystrophy with associated pain, movement disorder, and autonomic
dysfunction. Here is a review article describing the disorder:
Schwartzman RJ. Reflex sympathetic dystrophy. Current Opinion in
Neurology & Neurosurgery. 6(4):531-6, 1993 Aug.
"Reflex sympathetic dystrophy is a progressive illness most often
initiated by trauma to a nerve, plexus, or soft tissue. Its five
components are pain, edema, autonomic dysfunction, movement disorder,
and trophic changes. The illness evolves in stages that progress
insidiously over time. The length of time a patient remains in a
specific stage is unknown. In any stage of reflex sympathetic
dystrophy, the symptom complex may be dissociated. Reflex sympathetic
dystrophy occurs in one part of the body that seems to sensitize a
patient so that a succeeding injury may initiate the process in the
newly traumatized area. The length of time this sensitization lasts is
unknown. Pain is the most disabling and the most difficult aspect of
the illness to treat. At least in early stages the pain is
sympathetically maintained, but with time becomes sympathetically
independent. The alpha-1 adrenoreceptor appears to be the peripheral
link that, when activated, sensitizes directly or indirectly
C-nociceptor fibers. Dynamic mechanoallodynia is mediated by A beta
low threshold mechanoreceptors, whereas static primary mechanical
hyperalgesia may be mediated by sensitized C-nociceptors. A peripheral
afferent C-nociceptor input appears to be necessary to alter the
dorsal horn central processing mechanisms to allow for the expression
of dynamic mechanoallodynia. This nociceptive barrage could be driven
by the sympathetic efferent outflow or could be sympathetically
independent. The response of immediate early response genes may change
the neuropeptide concentration of the dorsal horn. Central
sensitization mediated by excitatory amino acids, neuropeptides, and
the N-methyl-D-aspartate receptor may be responsible for the severe
pain seen in the later stages of the illness. "
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I hope this information is helpful. Please feel free to ask for
clarification or post any other information you may recall about the
article you found if it is not among those listed above.
Best,
-welte-ga |
