UMEM Educational Pearls - Neurology

• Idiopathic Intracranial Hypertension, previously known as pseudotumor cerebri, can be treated with medications such as carbonic anhydrase inhibitors (i.e. acetazolamide), corticosteroids, indomethicin, loop diuretics, and analgesics used to treat migraine headaches.

• While removing excess cerebrospinal fluid (CSF) via lumbar puncture (LP) is sometimes considered to be an appropriate therapeutic intervention for IIH in the emergency department, it is generally not recommended for the following reasons:

             -- CSF reforms within 6 hours, making its removal short-term, unless there is a CSF leak.

             -- LP can be challenging in obese patients and uncomfortable for patients, in general.

             -- LP complications such as low pressure headaches, CSF leak, CSF infection, and intraspinal epidermoid tumors.

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• Many neurologic conditions present with motor dysfunction.  It is often helpful to distinguish these movement abnormalities in order to properly recognize and manage the disorder.
• Chorea >>> Sudden, ballistic movements.
• Athetosis >>> Writhing, repetitive movements.
• Fasiculations >>> Fine twitching of individual muscle bundles, most easily noted on the tongue.
• Dystonia >>> Sudden, tonic contractions of muscles of the tongue, neck (torticollis), back (opisthotonos), mouth, or eyes (oculogyric crisis).
• Tardive dyskinesia >>> lip smacking, chewing, and teeth grinding (early signs).

Optimal management of subarachnoid hemorrhage requires prognostic understanding and effective communication with neurology and neurosurgical consultants, as well as the patient and their family members.

It is therefore often helpful to utilize and reference the widely recognized Hunt and Hess Scale in grading symptoms of ruptured cerebral aneurysm and subarachnoid hemorrhage severity:

• Grade 1:  Asymptomatic; or minimal headache with slight nuchal rigidity.  Approximate survival rate (ASR) 70%.
• Grade 2:  Moderate to severe headache; nuchal rigidity; no neurologic deficit except cranial nerve palsy.  ASR 60%.
• Grade 3:  Drowsy; minimal neurologic deficit.  ASR 50%.
• Grade 4:  Stuporous; moderate to severe hemiparesis; possible early decerebrate rigidity and vegetative abnormality.  ASR 20%.
• Grade 5:  Deep coma; decerebrate rigidity; moribund. ASR 10%.
• Grade 6:  Death; brain dead.

For your convenience, an online Hunt and Hess Scale calculating tool can be found at:

http://www.mdcalc.com/hunt-and-hess-classification-of-subarachnoid-hemorrhage-sah

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Classic Cerebrospinal Fluid Characteristics

• Bacterial Meningitis >> Milky CSF with increased protein, decreased glucose, high WBC's, few RBC's, mildly increased opening pressure, normal % gamma globulin.

• Viral Meningitis >> Cloudy CSF with increased protein, normal glucose, increased WBC's (lymphocyte predominant), no RBC's, normal opening pressure, normal % gamma globulin.

• Herpes Simplex Encephalitis >>  Cloudy CSF with increased protein, normal glucose, increased WBC's (lymphocyte predominant), few RBC's, increased opening pressure, normal % gamma globulin.

• Subarachnoid Hemorrhage >> Yellow CSF with increased protein, normal glucose, few WBC's, inumerable RBC's, mildly increased opening pressure, normal % gamma globulin.

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• A broadly-accepted, standard definition of concussion, also known as mild traumatic brain injury (MTBI), does not exist and is still a work in progress. 

• Historically, the diagnosis of concussion has been based upon the presence of three findings:  (1) Loss of consciousness (usually for less than 30 seconds), (2) post-traumatic amnesia (usually for less than 24 hours), and (3) a Glascow Coma Scale score of 13 to 15.                  

• Today, many experts question whether loss of consciousness is inherently associated with concussion, but rather that any change in consciousness, such as that related to amnesia, suffices.  

• Patients with the following symptoms should be screened, typically with head CT, for more serious injury:  loss of/deteriorating consciousness, persistent headache, dizziness, vomiting, disorientation/confusion, seizure, and unequal pupil size.

• Treatment of concussion consists of monitoring and rest.  Symptoms usually spontaneously resolve within 3 weeks, but may persist for up to around 3 months.

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• When emergently managing stroke, be vigilant about anticipating potential complications and recognizing them with expediency, regardless of whether the patient receives tPA therapy.

• The following are associated with greater risk of developing cerebral edema and/or post-tPA hemorrhage:

              ---  High NIH Stroke Scale scores.

              ---  Large areas of infarct.

              ---  Cerebellar infarcts.

              ---  Extended time to tPA administration.

              ---  Previous stroke.

              ---  Older age.
 

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• Emergency department evaluation of diplopia is largely based on a comprehensive history and should always include the following questioning with documented findings:

1. Does the diplopia resolve by covering one eye?  (Differentiates binocular diplopia (disappears when one eye covered; most common) from monocular diplopia (persists with one eye covered; usually related to a focal, ocular problem).
2. Does the degree of diplopia change with direction of gaze and/or head position?  (Determines whether deficit related to cranial nerve innervation, helps localize associated paretic muscle).
3. Is the diplopia horizontal (i.e. two objects side by side) or vertical (i.e. two objects one on top of the other)?  (Horizontal diplopia suggests cranial nerve III or VI deficit (i.e. lateral gaze function); vertical diplopia suggests cranial nerve IV deficit (i.e. elevator or depressor gaze function).
4. Is there associated pain? (Suggests possible foreign body or extraocular muscle entrapment).
5. Was there associated trauma? (Blow-out fractures can be associated with diplopia).
6. Is there associated weakness, headache, confusion, or dizziness?  (Imaging usually indicated to rule out intracranial processes such as stroke or increased intracranial pressure).

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Chlorhexidine (CHG) has rapidly become the antiseptic of choice for most skin preparation prior to any percutaneous procedures including:

• venipuncture
• laceration repair,
• joint aspiration
• lumbar puncture???

The Chlorprep^(R) label notes: "DO NOT USE FOR LUMBAR PUNCTURE OR IN CONTACT WITH THE MENINGES" (attached)

Authors of the British Royal College of Anaesthetists 3rd National Audit Project provided some guidance for the use of chlorhexidine for spinal procedures

• Clinicians must take care to prevent CHG from reaching the CSF
  • Keep CHG away from other drugs and equipment being used
  • Allow solution to dry prior to beginning procedure
  • Avoid using solutions > 0.5% chlorhexidine
• Further comments
  • Chlorhexidine 0.5% in alcohol 70% is the optimal skin preparation for neuroaxial procedures
  • Risk of vertebral canal sepsis is greater than the very rare risk of neurotoxicity and arachnoidits from chlorhexidine
  • This is OFF-LABEL use and should be instituted formally at a departmental level with an audit process for complications

Further: Correspondance from the Journal of  Regional Anesthesia and Pain Medicine

"Dr. David Hepner published a correspondence in the April 2007 issue of Anesthesiology that stated the expert panel for Regional Anesthesia and Pain Medicine “felt strongly that although the US Food and Drug Administration has not approved chlorhexidine before lumbar puncture, it has a significant advantage over povidone iodine because of its onset, efficacy, and potency” and commented that “interestingly, povidone iodine is also not approved for lumbar puncture."

Chlorhexidine off-label use is supported in academic literature.  Due to specific labeling prohibiting use, a formal institutional policy to support such use may be indicated.

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Attachments

• 1008270020_chlorprep_instructions.pdf (293 Kb)

• When examining the hand, it is always important to document assessment of the ulnar, median, and radial nerves.
• The motor function of the hand can quickly and simply be assessed with the following examination techniques:
• Ulnar motor function >> Ask patient to first turn hand prone and spread fingers apart to a maximal distance.  Then, ask the patient to resist your attempts to squeeze the fingers together.
• Median motor function >> Ask patient to touch the distal tip of the thumb to the distal tip of the fifth finger and hold it.  Then, attempt to pull the two fingers apart and ask patient to resist.
• Radial motor function >> Ask patient to extend the wrist (i.e. as if trying to stop traffic) and push back against you attempting to push the hand into the flexed position.

• The largest and most commonly injured peripheral nerve of the upper extremity is the radial nerve.
• Radial nerve palsy presents with decreased dorsal sensation, poor extensor motor strength, and a deficit in the abduction of the arm and/or hand. The degree of disability depends on where the injury takes place along the course of the nerve and its extent.
• Patients presenting with radial nerve palsy often erroneously think that they have suffered a stroke, given the severe degree of flaccidity and functional loss that typically results.
• Emergency department management of radial nerve palsy consists of splinting the wrist in a slightly extended position, along with physical and occupational therapy, and Orthopedic/Hand follow up as needed.

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How to Perform a Median Nerve Block

• The most common emergency department indication for performing median nerve blocks is to anesthetize its hand distribution (i.e. volar surface of hand) for pain control and/or to perform procedures such as laceration repair and dislocation reductions.
• The median nerve is located at the proximal flexor crease of the wrist, between the palmaris longus (PL) and flexor carpi radialis (FCR) tendons.  The FCR lies radial to the PL tendon.
• Use a 25 or 27 gauge needle, inserted to a depth of 1 cm, to inject 3-5 mL of plain lidocaine proximal to the distal wrist flexor crease, just ulnar to the PL tendon.
• If the PL tendon is absent, as is the case in 25% of people, direct the needle in line with the ring finger.
• If distal paresthesias result, withdraw and reposition the needle as this suggests that the median nerve was directly struck, which should be avoided.

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• Ulnar nerve blocks are relatively easy to perform and excellent for anesthetizing the ulnar nerve distribution, particularly of the hand.

• Ulnar nerve blocks can be performed at the level of the wrist (dorsal or volar side) or at the elbow.  Volar side blocks at the wrist tend to be easier to perform and associated with less risk. 

• Using a 27 gauge needle, infiltrate 2 to 3 mL's of lidocaine between the flexor carpi ulnaris tendon and the distal-most aspect of the ulnar bone.  The needle should be inserted 1 to 2 cm's at about a 40 degree angle, at the proximal-most wrist crease.

• Do not puncture the actual ulnar nerve or the ulnar artery.  Should needle insertion cause distal hand paresthesias or blood withdrawal, do not inject and immediately remove the needle, as this suggests that the ulnar nerve or artery was struck, respectively.  The objective is to allow the lidocaine to infiltrate into the nerve, not to inject it directly into the nerve.

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• When examining the hand, care should be taken to thoroughly assess both the sensory and motor function on both the dorsal and palmar surfaces.

• The dermatomes of the hand provide sensation and are comprised of the ulnar, median, and radial nerves (see diagram below).

• (1) Light touch, (2) sharp touch (i.e. pinprick), (3) temperature, (4) propioception (joint position sense), (5) vibration, and (6) 2-point discrimination in the following nerve distributions should be assessed:

              --  ulnar nerve >>> supplies palmar surface and dorsal tips of little finger and medial half of ring finger, including

                   adjacent parts of hand.

              --  median nerve >>> supplies palmar and dorsal aspects of thumb, index finger, middle finger, and lateral half

                   of ring finger, including adjacent parts of hand.

              --  radial nerve >>> supplies most of dorsal surface of hand.

• Cervicogenic headaches are a syndrome of chronic, hemicranial pain that is referred to the head from bony structures or soft tissue of the neck.
• Adequate treatment of these headaches is often difficult to achieve, particularly from the emergency department, as a multi-faceted approach including pharmacologic, physical, anesthetic nerve block, psychological and sometimes surgical therapy, is often required.
• The emergency physician may prescribe simple agents such as acetaminophen and ibuprofen, with or without muscle relaxants to treat cervicogenic headaches.
• When close follow up is ensured, low doses of tricyclic anti-depressants or anti-epileptics such as gabapentin, divalproex sodium, carbamazepine, and topiramate may be utilized; while these are not FDA approved for the treatment of cervicogenic headaches, they have been shown to be effective for some headache types and neurogenic pain syndromes.

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Consider the diagnosis of a Cervicogenic Headache when the following findings are present:

A. Pain localized to the neck and occipital region, potentially with projection to forehead, orbits, temples, vertex or ears.

B. Pain is precipitated or aggravated by particular neck movements or sustained postures.

C . At least one of the following:

1. Resistance to or limitation of passive neck movements.

2. Changes in neck muscle contour, texture, tone or response to active and passive stretching and contraction.

3. Abnormal tenderness of neck muscles.

D. Radiological imaging reveals at least one of the following:

1. Movement abnormalities in flexion/extension.

2. Abnormal posture.

3. Fractures, congenital abnormalities, bone tumors, rheumatoid arthritis or other distinct pathology (not spondylosis or osteochondrosis).

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Cluster headaches are defined as a group of at least five headache attacks causing unilateral orbital, supraorbital and/or temporal pain, with at least one of the following simultaneous associated findings on the affected side:

1. conjunctival injection
2. lacrimation
3. nasal congestion
4. rhinorrhea
5. ptosis
6. miosis
7. sweating on the forehead

Cluster headaches can occur at a frequency of one every other day t  eight episodes per day.

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Migraine with aura (MA) diagnostic criteria

A. At least two attacks with at least 3 of the following:

1. One or more fully reversible aura symptoms (indicates focal cerebral cortical and/or brain stem functions).

2. At least 1 aura symptom develops gradually over greater than 4 minutes, or 2 or more symptoms occur in succession.

3. No aura symptom lasts greater than 60 minutes.

4. Headache follows aura with free interval of at least 60 minutes.

B. At least 1 of the following aura features establishes a diagnosis of migraine with typical aura:

1. Homonymous visual disturbance.

2. Unilateral paresthesias and/or numbness.

3. Unilateral weakness.

4. Aphasia or speech difficulty.

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• Several medications such as dopamine-blocking anti-emetics, triptans, and ergotamine derivatives have been shown to more effectively treat migraine headaches over other types of headaches, making the ability to accurately recognize this common (2.2% of all ED visits) condition essential.

• According to the International Headache Society, one meets diagnostic criteria for migraine headache without aura when they have experienced at least 5 attacks, each lasting 4 to 72 hours (untreated or unsuccessfully treated) and accompanied by at least 2 of the 4 following characteristics ("PUMA"):

          A.

              1.  Pulsatile or throbbing in quality

              2.  Unilateral in location

              3.  Moderate to severe in intensity

              4.  Aggravated by activity (i.e.climbing stairs, exertion), plus

         B.  at least 1 of the following 2 during the headache  ("VP"): 

              1.  Vomiting and/or nausea

              2.  Photophobia and/or phonophobia

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• Lacunar infarcts affect the deep penetrating vessels of the middle cerebral artery and carry the best prognosis of all strokes.

• There are 4 classic syndromes characteristically caused by lacunar infarcts, with which the emergency physician should be familiar and able to recognize.  They are:

1. Pure motor hemiparesis.
2. Pure sensory syndrome.
3. Ataxic hemiparesis (ipsilateral cerebellar and motor symptoms).
4. Clumsy hand dysarthria syndrome (ipsilateral hand weakness, patient may say their hand "feels awkward," dysarthria more pronounced than the weakness).

• The ability to detect brain CT abnormalities suggestive of ischemic stroke largely depends upon the time between the onset of symptoms and the CT examination.

• Large, cortical strokes are typically not detected on CT for at least 3 hours; Nearly 60% of strokes, however, are detectable on CT within 24 hours from time of infarct, and essentially 100% within 7 days.

• Clinical correlation:  Be sure that the reported time of symptom onset properly correlates with brain CT findings, as this could affect the decision to treat with tPA in accordance with appropriate time windows.  If a patient reports 1 hour of stroke symptoms, for example, and the brain CT shows significant edema and loss of gray/white matter differentiation suggesting infarct, be wary of a time discrepancy.

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