Making Sure Pedicle Screws are Correctly Placed During Spine Surgery

 During a spinal fusion, two or more vertebra are fused together in orrder to eliminate abnormal motion caused by degenerative conditions.

A spinal fusion may require stabilization of the lumbar spine using artificial devices (known as “instrumentation”) including wires, rods, plates and vertebral cages.

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This instrumentation is usually fixed to the vertebral body with a pedicle screw, as can be seen in the adjacent lateral radiograph.

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The pedicle screw is inserted through the bony lumbar pedicle, into the anterior vertebral body.

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These screws are inserted blindly from the back, similar to nailing the back panel on a book case, and just like with the book case, it’s easy to get off track:

Remember the last time you put a book case together – you nailed the back panel onto the frame (or where you thought the wood frame was), then flipped the whole thing over and found that many nails had missed.

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Obviously, a misplaced screw can end up inside the spinal canal, where it could injure the adjacent nerve roots, a potential cause of post operative deficit:

Various degrees of misplaced pedicle screws, and then (right) a pathologic specimen showing a pedicle wall that has been perforated by a pedicle screw

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As many as 70% of patients undergoing spinal fusion with instrumentation may have a misplaced screw, although most are just misplaced by a millimeter or two, and only 5-10% of those misplaced screws are cause for concern.

However, the incidence of an actual new neurologic deficits from a misplaced screw is much lower, estimated at less than 2 per 1000 screws in a recent study.

Nevertheless, this is still cause for concern, because it may be difficult to detect a misplaced screw during surgery.   Pedicle screw placement may be checked by:  Direct inspection and palpation, Fluoroscopy, Electrical testing, Computerized navigation or the Pediguard system.

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If the surgery involves a laminectomy, then the spinal canal will be open, and the surgeon will either see the misplaced screw, or feel it when they swipe a finger along the medial pedicle wall.

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However, in most cases, there is no laminectomy required, and doing so would prolong surgery time unnecessarily, so misplaced screws can go unrecognized.

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Intraoperative fluoroscopy (live X-rays taken during the operation) can detect most pedicle wall perforations and misplaced screws, but is only about 75% accurate because of limited available two dimensional viewing planes.  Furthermore, excessive use can expose the patient to excessive radiation.

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Real time electrophysiologic testing has been used in the operating room to confirm correct placement of pedicle holes and screws during surgery.

The premise here is that a pedicle screw or hole that is correctly placed within the wall of the bony pedicle (b, above), will be separated from the adjacent nerve root by a layer of cortical bone which has a high impedance (resistance) to the passage of electrical current.

However, a pedicle hole or screw that has perforated the medial bony wall of the pedicle (a, above), will lie directly adjacent to the nerve root without that intervening layer of cortical bone.

Hence electrical stimulation of that perforated hole or screw (a) is more likely to activate the adjacent nerve root and evoke a recordable muscle twitch in the innervated muscle (a) at a lower stimulus intensity (threshold)  than in case of the correctly placed hole or screw (b).

This electrical threshold testing has become very popular, but requires the presence of specialized equipment and personal in the operating room.

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New “O-arm” technology allows computed tomographic images to be fused with a computerized navigation system, allowing 3 dimensional visualization of pedicle screw tracks as they are inserted in the operating room:

However, this technology is expensive, and may not be widely available.

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And finally, the Pediguard, a simple, cheaper and widely available technique that uses a disposable hand held drill that emits a signal based on the thickness of surrounding bone, and can be used by any surgeon in any operating room to ensure correct placement of pedicle screws in real time without the need for extra specialized equipment or personnel.

Anisocoria (Unequal pupils)

The pupil is the hole in the center of the iris, that allows light to enter the retina. The iris is a thin strip of smooth muscle which regulates the amount of light entering the eye by controlling the size of the pupil.

The iris actually consists of two smooth muscles:  There is a circular group called the sphincter pupillae, which is innervated by the parasympathetic fibers that travel with the oculomotor nerve, and when activated constricts the pupil. There is also a radial muscle group called the dilator pupillae, innervated by sympathetic nerves from the superior cervical ganglion, which when activated causes the pupil to dilate.

Anisocoria (unequal pupils) can be physiologic, or can result from a variety of disorders of the nervous system.

Anisocoria – the pupils are unequal, is the the pupil too large, or is the left pupil too small?

The first step in evaluating anisocoria is to determine which is the abnormal side – this can be accomplished by comparing the pupil sizes in response to bright light and dull ambient light:

If the smaller of the pupils is abnormal, a miosis, then the anisocoria will be more apparent (the affected pupil will be smaller) in dull ambient light conditions (a dark room), and less apparent (the pupils will be more equal) in bright light.

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Alternatively, if the large pupil is the abnormal side, mydriasis, it will fail to contract in response to intense light.

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Miosis (small pupil)

A unilateral miosis can be physiologic or can indicates a lesion affecting the sympathetic nerve fibers to the eye known as Horner’s syndrome.

Physiologic anisocoria is mild (usually less than 0.5 mm difference in size between the pupils, and the amplitude of the difference does not vary greatly under dim or bright light conditions.

Horner’s syndrome causes unilateral miosis, and the affected abnormal pupil either does not dilate or has a delayed dilation in the dark. Furthermore, there is usually an associated lid ptosis and facial hypohidrosis. Horner’s syndrome is important to diagnosis, because it can indicate a lesion in the brain stem (stroke), neck (carotid artery dissection) or lung apex (Pancoast’s tumor).

Right Horner’s syndrome (ptosis and miosis), from R apical lung tumor (Pancoast tumor).

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Mydriasis (Dilated Pupil)

This is most commonly caused by an anticholinergic drug, such as atropine or hyoscyamine, hyoscyamine, either from a medication, eye drop or misplaced nebulizer:

Unilateral mydriasis, caused by direct anticholinergic drug effect on iris because of a badly fitting face mask.

Damage or compression of the oculomotor nerve buy an aneurysm or brain herniation can also cause mydriasis, typically associated with ptosis and ophthalmoparesis:

R ptosis, occulomotor palsy (eye is deviated down and outwards), with a dilated pupil, caused by nerve compression from aneurysm (red arrow)

Mydriasis from Adie’s Syndrome

Adie’s syndrome presents with abrupt onset mydriasis often associated with loss of deep tendon reflexes, thought to be the result of a viral infection that causes damage to neurons in the ciliary ganglion (the area of the brain that provides parasympathetic control of eye constriction). Clinical exam may reveal sectoral paresis of the iris sphincter or vermiform iris movements:

American Academy of Neurology Identifies 5 Questionable Practices

It’s no secret that health care costs are escalating.

Although physicians value their independence, part of the problem here is the unregulated use of costly tests, medications and procedures, many of which are unproven and of questionable benefit.

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Evidence based medicine assess the strength of the evidence of risks and benefits of treatments (including lack of treatment) and diagnostic tests in an attempt to help clinicians predict whether a treatment will do more good than harm.

However, less than 1 in 5 medical decisions in the USA are made based on evidence-based medicine.

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The American Academy of Neurology has recently taken a step in the right direction by publishing a list of 5 costly neurology practices which continue to be widely performed despite being of little proven benefit:

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1. Don’t perform electroencephalography (EEG) for headaches.

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2. Don’t perform imaging of the carotid arteries for simple syncope without other neurologic symptoms.

Syncope is caused by global cerebral hypoperfusion, not carotid artery disease, so even if a carotid stenosis is identified, it would be asymptomatic (see point number 5)

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3. Don’t use opioid or butalbital treatment for migraine except as a last resort.

Butalbital is effective short term treatment for migraine, but commonly leads to rebound, which ultimately exacerbates migraine.  Click here for more information about migraine.

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4. Don’t prescribe interferon-β or glatiramer acetate to patients with disability from progressive, nonrelapsing forms of MS.

Interferon-β and glatiramer acetate, are effective for  relapsing phases of MS, but do not prevent the development of permanent disability in progressive forms of multiple sclerosis.  These medications cost more than $40,000 a year, and put a financial strain on the patients and their families to make the co-pays.  In some series as many as 10%-15% MS patients have progressive forms of the disease and yet are still taking one of these medications.

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5. Don’t recommend carotid endarterectomy (CEA) for all patients with asymptomatic carotid stenosis.

Surgery is of much less benefit for asymptomatic carotid stenosis, and should be reserved for those with a perioperative complication risk of less than 3% and a life expectancy of greater than 3 to 5 years. Click here for more information about surgery for carotid artery disease.

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Click here for more details.

Intrathecal Baclofen Infusion For Spasticity

Posted by Ilya Shnaydman, Drexel University College of Medicine Class of 2013:

Spasticity is defined as a ‘stiffness’ or ‘tightness’ of muscle due to spasms, or increased muscular tone. It is usually due to a lack of inhibition, as seen in an upper motor neuron lesion affecting the brain or spinal cord. Examples of upper motor neuron lesions include stroke (cerebrovascular infarct), multiple sclerosis, traumatic brain injury and cerebral palsy.

Although the exact cause of spasticity is not know, it is theorized to be due to an imbalance between the excitatory and inhibitory input to a muscle group. Increased excitability leads to spasticity, whereas increased inhibition leads to a flaccid muscle.

This can be better understood by illustrating the popular ‘knee jerk reflex’. During this test, the examiner strikes the patellar ligament with a reflex hammer which stretches specialized sensory fibers called the muscle spindle. This produces a signal which travels to the spinal cord (specifically at the L4 level). From the spinal cord, another specialized nerve complex called the ‘alpha-motor neuron’ conducts an impulse back to the quadriceps femoris muscle which triggers the contraction (knee jerk).

One of the patients treated at Monmouth Medical Center by the Neurology Specialists of Monmouth County, TM (the patient’s name is hidden to preserve anonymity)  is a 65 year old male who suffers from a spinal cord infarct 15 years ago, which resulted in spasticity of his lower extremities (legs) just as described above. The right side has been affected more than the left.  He has difficulty walking, as his gait is very rigid, but does manage to get around using a cane.

For spasticity, medical treatment consists primarily of physical therapy and muscle relaxants such as baclofen, benzodiazepines, and even botulinum injections. When these methods have been exhausted and either do not work to the patient’s satisfaction or cause side effects, patient’s must turn to experts in the treatment of spasticity.

The patient’s multidisciplinary neuroscience physicians at Monmouth Medical center urged the patient to consider intrathecal baclofen to help the patient improve his gait and overall quality of life. By injecting baclofen directly into the spinal canal (where the spinal cord lays), his neurologists are able to give significantly lower doses of the medication (as it directly contacts the spinal cord) and prevent unwanted side effects.

Baclofen is infused into the spinal canal via a programmable pump that is implanted beneath the skin (similar to a pacemaker). The pump’s batteries last about 10 years and most patients do not notice any discomfort from having the pump implanted. The baclofen is replenished by injecting it into the pump’s port (yellow arrow) with a small needle.

Before undergoing surgery for placement of the baclofen pump, patients typically undergo a trial to see if the intrathecal baclofen will be beneficial to them. During this ‘trial’, baclofen is injected directly into the spinal canal during a spinal tap (lumbar puncture, or needle placed through the skin into the spinal canal). The patient is then observed over a few hours to see if they are a good candidate for the permanent intrathecal baclofen pump. During the trial, only a small dose of baclofen is used, so once the pump is placed and programmed, the patient can expect to see even more benefit from the therapy. After the pump has been placed it can be adjusted non-invasively using a magnet (similar to a pacemaker) and should be followed by a neurologist to adjust the dosage as needed.

Below you can see the effect of the baclofen trial (again with just a small dose) for our patient, TM

Alice in Wonderland Syndrome

Caused by a disturbance of perception rather than an actual physiological change
– Altered body image (Ex: big buildings look same size as person’s own body)
– Distorted perception of size (micropsia, macropsia)
– Distorted perception of the shape of objects
– Loss of spatial perspective (sense of time and space)
– Auditory or tactile hallucinations

AIWS generally affects a younger population and has several associated conditions. Migraine is the classic disease linked to AIWS, the distorted sensations can either begin before a migraine (aura or “warning”) or afterwards, and in younger patients can even occur without headache

Check out these first-hand accounts of people with this interesting phenomenon:
Size Matters: Living in a Lewis Carroll ‘Wonderland’ – ABC News

When the world looks like a real-life Wonderland

Experience: I have Alice In Wonderland syndrome 

A Not So Pleasant Fairy Tale: Investigating Alice in Wonderland Syndrome | Serendip Studio

Other causes of Alice in Wonderland Syndrome are:
psychoactive drugs
infectious mononucleosis
malignancy
temporal lobe epilepsy

Certain tests & imaging studies help rule out secondary causes:
– urine toxicology screen
– monospot test   (for mononucleosis)
– MRI brain – with and without contrast (to look for malignancy)
– EEG   (to detect seizures or seizure-like activity)

Sounds scary, right? Well, good news is it’s not as bad as it sounds. Most patients who experience AIWS as children will outgrow the condition as adults. Patients should be monitored for worsening of symptom severity and frequency. If all studies are negative and the patient continues to improve clinically, then further evaluation and/or treatment is not needed. Best management for future attacks is focused on migraine prophylaxis and lifestyle modifications (healthy diet, regular exercise, adequate sleep).

Posted By Sidra Ghafoor, Drexel University College of Medicine Class of 2013

Epilepsy and Seizures, What’s the difference?

What is a Seizure?

A seizure (or “fit”) is physical finding or change in behavior that occurs because of abnormal electrical activity in the brain.

When people think of a seizure, they usually imagine a generalized (or “Grand Mal”) tonic clonic seizure:

It is estimated that as many as 5% of all Americans will experience an epileptic seizure during their lifetime.
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What is epilepsy?

Epilepsy results from a permanent change in brain tissue causing it to be too excitable, leading to repeated unpredictable seizures over time.

This can occur from a brain injury, such as head trauma, birth asphyxia or a stroke, brain tumor or can be genetic (something you were born with).

The prevalence of epilepsy is estimated to be 1-2% in the USA.

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Not all seizures lead to epilepsy.

Why is the prevalence of epilepsy so much lower than the incidence of seizures?

The answer is that not all seizures will lead to epilepsy.

A seizure can be provoked by some extraneous factor such as high fever, medication, drugs and alcohol, or blood electrolyte disorder, which if addressed properly will not lead to further seizures.

However, a single seizure can also be the beginning of epilepsy, necessitating an anti-epileptic medication (or anticonvulsant) to prevent further episodes.

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So, how do you tell if a first seizure is the beginnings of epilepsy?

All patients presenting with their first seizure should have a thorough evaluation, including a detailed history (from someone who observed the episode), physical examination, blood work, brain imaging study and electroencephalogram.

A seizure which begins with a focal onset, such as a warning (“aura”), unusual behavior (“automatism”), or focal movements just as turning the head to one side or jerking on one side of the body suggests the beginnings of epilepsy from an underlying brain injury or lesion.

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Seizure with automatism (Partial Complex Seizure):

Note that the patient appears awake, but is not responding normally, and has lip smacking and pointing (the automatisms), indicating a focal (temporal lobe) seizure onset.  He seems confused and disoriented afterwards.

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Seizure with focal motor activity:

Although the patient is unresponsive and jerking, note that the head is turned to the right and there are only right sided limb movements, indicating that the seizure is coming from the left side of the brain.

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Some genetic seizure syndromes, like juvenile myoclonic epilepsy or absence epilepsy (“petit mal”) begin in childhood or adolescence, are associated with characteristic EEG findings, and indicate epilepsy which will be recurrent without treatment.

Absence seizure:

The child is talking, then suddenly stops and stares off into space, then suddenly resumes speech as if nothing happens. This is a typical absence seizure or “Petit Mal” from epilepsy and will recur without treatment.

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There are physical signs which suggest an underlying neurocutaneous syndrome, and epilepsy:

Syndrome characterized by a facial port-wine stain, seizures, paralysis or weakness on one side, learning disabilities, and “calcification” in the brain

Genetically determined syndrome of epilepsy associated with: Red patches on the face containing many blood vessels (adenoma sebaceum) . Areas of the skin that are white (due to decreased pigment) and have either an ash leaf or confetti appearance . Raised patches of skin with an orange-peel texture (shagreen spots), often on the back . Small tumor like lesions at the nail folds (subunguual fibromas) .

Genetically determined epilepsy syndrome associated with fatty tumors, pigmented patches (including in the arm pits), and Lisch nodules in the iris.

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The presence of an abnormal EEG in a patient presenting with a single seizure increases the chances of another seizure (epilepsy) and may warrant initiation of an anticonvulsant medication. This could be either a focal spike suggesting a partial onset seizure focus:

Or a burst of generalized spike wave activity, suggesting a genetic generalized epilepsy:

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A patient with seizures and an abnormal brain imaging study is also more likely to suffer a recurrence and develop epilepsy:

However, if all the tests are normal, it can be hard to tell if a single unprovoked seizure is the beginning of epilepsy or not, only about 20-30% of these patients will have a recurrent event, so sometimes it is better to wait and see what is going to happen rather than rushing into starting an anticonvulsant medication here.

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Where to get more help.

These are complicated issues and decisions which should only be made after consultation with a neurologist, preferably a neurologist with subspeciality training or certification in epilepsy at an epilepsy center.

Is it OK to take a generic medication?

A “generic” is a drug that is broadly equivalent to a brand name medication, but marketed under its chemical name, without advertising, usually at a significantly lower cost.

In most cases, generic products are available once the patent protections afforded to the original developer have expired, and when this happens free market competition leads to substantially lower prices for both the original brand name product and the generic forms.

Insurance companies and pharmacies will try to contain their own costs by encouraging patients to switch to generic medications with lower co-pays or co-insurance.

A generic drug must contain the same active ingredients as the original formulation. According to the FDA, generic drugs are identical or within an 80-125%  bioequivalent range to the brand name counterpart.

Generic substitution is not usually a major problem for most medication prescribed for common medical conditions like high blood pressure or diabetes.

Generic substitution for epilepsy medications is more contentious.

The problem is that most pharmacies get generic medications from wholesalers, and a patient on generic medication could potentially get drug from a different manufacturer every month.

Think of going shopping for peanut butter at a wholesale store like Costcos.  One month they might have Smuckers brand, the next month Kirkland brand, and then the next month some other brand – they have whatever they could order cheapest that month.  While these products all contain peanut butter, they each have slightly different recipes and taste a little bit different.

If you are taking levitiracetam (the generic equivalent of Keppra) for epilepsy, and you switch drug manufacturers every  month, you could potentially go from a product that was 125% Keppra bioavailability to a product that was 80% Keppra bioavailability, i.e. a 45% drop in effective drug ingredient at the same “dose”, and this could provoke a breakthrough seizure, with all of the ramifications for safety and driving that would go along with that.

That’s the reason that most neurologists and the Epilepsy Foundation have suggested that well-controlled epilepsy patients stick with brand name medications, so that they know they are getting the same thing every month when they refill their prescriptions.

Thankfully, we are beginning to see new mail order pharmacies, like Nuro Pharma, that will guarantee that the patient receive their generic epilepsy medications from the same manufacturer every month – if you know you are going to get Kirkland every month, it’s probably OK to pass on the Smuckers!!

New Monmouth Neuroscience Clinic Space

The Neuroscience Institute at Monmouth Medical Center is proud to announce the opening of its brand new out-patient clinic space on the 4th floor of the Wimpfheimer building, which will will be the home of many new  innovative programs.

View of Monmouth from Third Ave, showing Wimpfheimer building (center).

This historical building was erected in 1919 with money donated by board of trustee member Charles A. Wimpfheimer, in memory of his 19-year old son Jacques, who when stricken with pneumonia while in military service requested that he be given the same treatment as the other privates, and as a result was sent to a ward in a Hoboken hospital, where he died.

DIRECTIONS:
Click here for directions to Monmouth Medical Center.

Once you arrive, enter the hospital from 3rd Avenue (1), park (2) and enter the hospital via the Radiation-Oncology Entrance (3).  Register at the desk:

You will be directed to elevators that will bring you up to the 4th floor (BBR4), where you will pass through a nursing evaluation, then proceed to out brand new out-patient space on Wimpfheimer 4.

Sciatic Neuropathy

The terms lumbar radiculopathy and sciatica are used interchangeably to indicate radiating pain, numbness and weakness in a leg from a pinched nerve root in the back.

However, it is important to recognize that similar symptoms and signs can be caused by injury or compression of the sciatic nerve outside the spine, either in the buttock or thigh.

The sciatic nerve is the longest and widest nerve in the body, extending from the spine all the way to the foot, and contributes most of the nerve supply to the leg:

Sciatic nerve injury presents with:

1. Numbness affecting the entire leg, aside from the front of the thigh.

2. Weakness of the hamstrings, and all movement at the ankle.

3. Absent ankle jerk.

http://www.youtube.com/watch?v=z2YrjAGChBw&feature=youtu.be&rel=0

Sciatic Nerve Injury in the Buttock:

The nerve can be injured by misplaced buttock injections, gunshot wounds and knife injury. Buttock injections should be given in the upper outer quadrant to avoid the sciatic nerve

The sciatic nerve injury can also be injured by prolonged sitting on a toilet seat, either from direct nerve compression or hemorrhage and compartment syndrome into the gluteal muscles.  This has been reported in cases of  severe prolonged diarrhea, or drug induced coma on the toilet, so called toilet seat neuropathy.

Sciatic Nerve Injury at the Hip:

The sciatic nerve runs behind the hip joint as it travels through the buttock.
The sciatic nerve is frequently injured by a posterior dislocation of the hip:

Sciatic nerve injury occurs in as many as 1%–3% of patients who undergo total hip replacement surgery, usually from a stretch injury to the nerves, but occasionally from a misplaced crew, broken piece of wire, fragment of bone or cement pressing on the nerve:

Sciatic nerve injury after hip arthroplasty. (a) The skin incision for the transgluteal approach is in a continuous line. The cross on the left shows the ischium and the one on the right shows the trochanter. Between them, the skin projection of the sciatic nerve is seen. (b) The sciatic nerve was freed from all attachments. The arrows identify acrylic material from the hip arthroplasty, which was damaging the nerve

Piriformis Syndrome:

However, symptoms of sciatic neuropathy most often result from nerve compression by the piriformis muscle at the level of the sciatic notch, so-called piriformis syndrome.

This presents with buttock tenderness and pain, radiate down the posterior thigh.  Symptoms are made worse by prolonged sitting, bending at the waist, and activities involving hip adduction and internal rotation.  The pain can be reproduced by deep palpation over the sciatic notch.

Diagnostic modalities such as CT, MRI, ultrasound, and EMG may all be normal in piriformis syndrome, but are still useful for excluding other conditions.

Magnetic resonance neurography is a specialized imaging technique which can confirm the presence of sciatic nerve irritation or injury of the sciatic nerve in the piriformis muscle.

MRN findings in piriformis syndrome. A: Axial T1-weighted image of piriformis muscle size asymmetry (arrows indicate piriformis muscles). The left muscle is enlarged. B and C: Coronal and axial images of the pelvis (arrows indicate sciatic nerves). The left nerve exhibited hyperintensity. D: Curved reformatted neurography image demonstrating left sciatic nerve hyperintensity and loss of fascicular detail at the sciatic notch (arrows).

Conservative treatment can include medications, physical therapy and stretching, or injection of a paralysing agent such as botulinum toxin into the piriformis muscle under ultrasound or CT control. Surgery may be necessary for recalcitrant cases.

Concussion Assessments at Monmouth

The Matthew J. Morahan, III Memorial Health Assessment Center for Athletes is now available at Monmouth Medical Center.

Concussion

What does this mean?

1. Monmouth will be offering baseline IMPACT screening and cardiac screening to high school and college athletes, either at a free screening event or by appointment.

2. Athletes who sustain a sports related concussion and require immediate medical attention will be evaluated in the Monmouth Medical Center Emergency Room.  If they are felt to be suffering from ongoing symptoms of concussion, they can be referred to the Monmouth Concussion Center for same or next day evaluation by a neurologist and return to play determination.

3. Evaluation in the Monmouth Concussion Center will typically include a physician assessment, simple balance testing and IMPACT (R) cognitive testing.

4. The results of these evaluations with be forwarded to the athlete’s primary physician and athletic trainer, and arrangements will be made for appropriate follow-up.

Click here for more information about concussion.

Click here for directions to the Monmouth Neuroscience Out-Patient Area.