The flashcards below were created by user
on FreezingBlue Flashcards.
Short note on Spinal shock. [TU 2060,59/12]
Spinal shock is defined as a loss of sensation accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI) – most often a complete transection
Phases of spinal shock?
Return of reflex activity below level of injury (such as bulbocavernosus) indicates end of spinal shock
Spinal shock does not apply to lesions that occur below the cord, and therefore, low lumbar burst fracture should not cause spinal shock (and in this situation, absence of the bulbocaveronsus reflex indicates that there is a cauda equina injury); persistent loss of the bulbocavernosus reflex may be a result of a conus medullaris injury (eg from an L1 burst #)
Return of the bulbocavernosus reflex (anal sphincter contraction in response to squeezing the glans penis or tugging on the Foley) signifies the end of spinal shock, and for complete injuries, further neurologic improvement will be minimal
Bulbocavernosus reflex involves the S1, S2, S3 neurve roots and is spinal cord mediated reflex; and its presence signals the end of spinal shock, and rarely will spinal shock last beyond 48 hrs
Complete absence of distal motor function (EHL - S1) or perirectal sensation, together with recovery of the bulbocavernosus reflex, indicates a complete cord injury, and in such cases it is highly unlikely that significant neurologic damage will return; and in contrast, any spared motor or sensory function below level of injury is considered an incomplete spinal cord injury
What is Cauda equina syndrome. [TU 2072]
The clinical condition arising from dysfunction of multiple lumbar and sacral nerve roots within the lumbar spinal canal. Usually due to compression of the cauda equina.
Etiologies of CES?
- 1. Compression of cauda equina
- A. Massive herniated lumbar disc
- B. Tumor
- i. From compression: e.g. with metastatic disease to the spine with epidural extension
- ii. intravascular lymphomatosis (B-cell lymphoma): a circulating lymphoma without solid mass.
- C. Free fat graft following discectomy
- D. Trauma: fracture fragments compressing cauda equina
- E. Spinal epidural hematoma
may cause neurologic deficit from compression (vertebral osteomylitis, Spinal epidural abscess) or vascular compromise (septic thrombophlebitis)
: ischemic or inflammatory
4. Ankylosing spondylitis
: etiology is often obscure
Clinical findings in CES?
- 1. Sphincter disturbance:
- A. Urinary retention: the most consistent finding. Cystometrogram (when done) shows a hypotonic bladder with decreased sensation and increased capacity.
- B. Urinary and/or fecal incontinence: some patients with urinary retention will present with overflow incontinence
- C. Anal sphincter tone: diminished in 60-80%.
3. Significant motor weakness
- 2. Saddle anesthesia: the most common sensory deficit.
- Distribution: region of the anus, lower genitals, perineum, over the buttocks, posterior-superior thighs. Once total perineal anesthesia develops, patients tend to have permanent bladder paralysis
: usually involves more than a single nerve root (if untreated, may progress to paraplegia)
4. Low back pain and/or sciatica
(sciatica is usually bilateral, but may be unilateral or entirely absent, prognosis may be worse when absent or bilateral
5. Bilateral absence of Achilles reflex
has been noted
6. Sexual dysfunction
(usually not detected until a later time)
Pattern of CES progression?
CES tends to develop either acutely, or (less typically) slowly (prognosis is worse in the acute onset group, especially for return of bladder function).
- There are 3 patterns:
- Group I - sudden onset of CES symptoms with no previous low back symptoms
- Group II - previous history of recurrent backache and sciatica, the latest episode combined with CES
- Group III - presentation with backache & bilateral sciatica that later develop CES
Management of CES?
Typically requires prompt surgical decompression (within about 8 hours of the onset of symptoms) in order to reduce or eliminate pressure on the impacted nerves. Surgery within 24 to 48 hours gives the maximum potential for improvement of sensory and motor deficits.
Best treated with decompression by a bilateral lumbar laminectomy
, but a lumbar microdiscectomy
may be used given a patient’s unique situation.
- Surgical options
- A) Transcanal approach
- - Lumbar laminectomy and dissectomy
- - Sequestrectomy - removal of only herniated portion of disc
- B) Intradiscal procedure
- - Chemoneurolysis (using Chymopapin)
- - Automated percutaneous lumbar dissectomy
- - Percutaneous endoscopic lumbar dissectomy
Short note on Trigeminal neuralgia. [TU 2065/5]
Trigeminal neuralgia (TN), also known as tic douloureux, characterized by recurrent brief episodes of unilateral electric shock-like pains, abrupt in onset and termination, in the distribution of one or more divisions of the fifth cranial (trigeminal) nerve that typically are triggered by innocuous stimuli.
Signs and symptoms of trigeminal neuralgia?
- Paroxysmal, stereotyped attacks of usually intense, sharp, superficial, or stabbing pain in the distribution of one or more branches of the fifth cranial (trigeminal) nerve.
- Pain is maximal at or near onset. Facial muscle spasms can be seen with severe pain. This finding gave rise to the older term for this disorder, tic douloureux.
- It usually lasts from one to several seconds, but may occur repetitively.
- A refractory period of several minutes during which a paroxysm cannot be provoked is common.
- Some patients with longstanding TN may have continuous dull pain that is present between paroxysms of pain.
- Unlike some other facial pain syndromes, TN typically does not awaken patients at night.
- TN is typically unilateral.
- The distribution of pain most often involves the V2 and/or V3 subdivisions of the trigeminal nerve.
- Autonomic symptoms, usually mild or moderate, can occur in association with attacks of TN in the V1 trigeminal distribution, including lacrimation, conjunctival injection, and rhinorrhea.
- Trigger zones in the distribution of the affected nerve may be present and are often located near the midline. Lightly touching these zones often triggers an attack, leading patients to protect these areas.
- Other triggers of TN paroxysms include chewing, talking, brushing teeth, cold air, smiling, and/or grimacing.
Causes of trigeminal neuralgia?
- Idiopathic - Most common
- Compression of the trigeminal roots by tumors or vascular anomalies may cause similar pain.
- Most commonly the superior cerebellar artery – compressing or throbbing against the microvasculature of the trigeminal nerve near its connection with the pons.
Diagnosis of TN?
No laboratory, electrophysiologic, or radiologic testing is routinely indicated for the diagnosis of TN, as patients with a characteristic history and normal neurologic examination may be treated without further workup.
Management of TN?
- Medications -
- 1. Anticonvulsants - carbamazepine has been shown to be effective in treating the condition.
- 2. Antispasmodic agents - Muscle-relaxing agents such as baclofen may be used alone or in combination with carbamazepine.
- 3. Botox injections injections may reduce pain from trigeminal neuralgia in people who are no longer helped by medications
- The goal of trigeminal neuralgia surgery is to stop the blood vessel from compressing the trigeminal nerve or to damage the trigeminal nerve to keep it from malfunctioning. Surgical options include:
- 1. Microvascular decompression - involves relocating or removing blood vessels that are in contact with the trigeminal root
- 2. Gamma Knife radiosurgery - focused dose of radiation to the root of trigeminal nerve to eliminate pain
- 3. Other procedures - rhizotomy (destruction of nerve fibers, which causes some facial numbness)
American Spinal Injury Association (ASIA) Impairment Scale?
A = Complete: No sensory or motor function is preserved in sacral segments S4-S5
B = Incomplete: Sensory, but not motor, function is preserved below the neurologic level and extends through sacral segments S4-S5
C = Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have a muscle grade of less than 3
D = Incomplete: Motor function is preserved below the neurologic level, and most key muscles below the neurologic level have a muscle grade that is greater than or equal to 3
E = Normal: Sensory and motor functions are normal
Structure of the peripheral nerve trunk?
- The nerve contain many axons which are supported by connective tissue structures.
- All axons are surrounded by Schwann cells.
- In myelinated fibres the Schwann cells form an insulating sheath, each Schwann cell being associated with only one axon.
- Integrity of the myelin sheath is necessary for conduction of nerve impulses in myelinated fibres.
- Unmyelinated fibres are composed of several axons wrapped by a single Schwann cell.
- The Schwann cell basement membrane, together with endoneurial collagen fibres, forms the endoneurial tube. Large numbers of nerve fibres are gathered in fascicles surrounded by a connective tissue sheath called the perineurium. The fascicles are bound together and the whole trunk ensheathed by a further connective tissue layer called the epineurium.
Response of a nerve to injury?
- If trauma to a nerve is sufficient to disrupt axons then the distal part of the nerve undergoes Wallerian degeneration.
- The axons in the proximal part of the nerve have the potential to regenerate into the endoneurial tubes of the distal segment and subsequently make connections with target organs.
- The regeneration proceeds slowly with axons growing at only 1—2 mm/day in humans.
Classify peripheral nerve injury. Outline the principle of management of peripheral nerve injury. [TU 2055,63,64,65]
Classification of nerve injuries
- The extent of damage to the supporting connective tissue layers influences the quality of recovery and is the basis of the classification of nerve injuries.
- The most widely used classification of nerve injuries was described by Seddon.
- There are three types of injury of increasing severity:
- 1. Neuropraxia (nerve not working) - Sundarland I - It is temporary physiological paralysis of nerve conduction.
- - Injury to myelin sheath only.
- - The axons are in continuity and therefore Wallerian degeneration does not occur.
- Nerve conduction distal to the site of injury remains normal.
- Neuropraxia is a relatively mild injury typically caused by moderate compression such as that caused by a tourniquet, slight stretching or the passage of a missile close to a nerve.
- Recovery is complete providing the cause is removed, but the time varies from days to several weeks.
- 2. Axonotmesis (axons divided) - Sundarland II-IV
- This represents an anatomical disruption of the axons and their myelin sheaths. However, the supporting connective tissue structures including the endoneurial tubes, perineurium and epineurium are still intact.
- Wallerian degeneration occurs distal to the site of injury and, hence, distal conduction is lost.
- Axonotmesis results from a more severe blow or stretch injury to a nerve. For example, radial nerve palsy associated with fracture of the humerus is usually an axonotmesis.
- Recovery occurs by axon regeneration proceeding at a rate of 1—2 mm/day.
- Axons regenerate along the same endoneurial tube and therefore connect with the same end organ as before injury.
- The prognosis is good, restoring near-normal sensory and motor function.
- 3. Neurotmesis (whole nerve divided) - Sundarland V
- Here complete division of nerve fibres with sheath occurs.
- Degeneration occurs proximally up to the first node of Ranvier as well as distal to the injury.
- Recovery is incomplete even after nerve suturing.
- There is complete loss of motor and sensory functions with loss of reflexes.
- If the nerve is mixed type other than pure motor or sensory recovery is still poorer.
Sunderland’s classification of nerve injury?
- In 1951 Sunderland defined five degrees of nerve injury on the basis of increasing anatomical disruption of the nerve trunk.
- I: Conduction block—temporary neuronal block
- II: Axonotmesis but endoneurium is preserved
- III: Axonotmesis with disruption of endoneurium, but perineurium is preserved
- IV: Here disruption of endo and perineurium has occurred but epineurium is intact
- V: Neurotmesis with disruption of endo, peri and epineurium has occurred
Clinical Features of nerve injury?
- Loss of sensory, motor, autonomous and reflex functions.
- Secondary changes in the skin and joint.
What is causalgia?
- This is a type of neuralgic pain associated with a major nerve injury which often may be partial.
- The pain is intense and burning in character. The pain, however, improves with recovery of nerve function.
Investigations for nerve injury?
- Associated injuries like fracture, vessel injury, injuries in other systems should be looked for.
- Assessment of nerve injury is done by checking sensation, muscle power, reflexes.
- Nerve conduction studies.
- Electromyography (EMG)
- Magnetic resonance imaging (MRI
- Investigations relevant for associated injuries.
Treatment of nerve injury?
- A. Timing of repair -
- - Primary repair - is the optimal approach for peripheral nerve injuries taking place within the first couple of days
- - Secondary repair takes place one week or more after the injury
- - Partial injuries (15% of injuries) as a consequence of stretch or contusions are commonly managed with secondary repair.
- - For complete injuries the method of repair depends on what is found during exploration. If the epineurium is found to be neatly divided then primary repair without tension is usually undertaken but if the ends are ragged then a graft may be required.
- B. Technique of nerve repair -
- There are four main steps to a primary end-to-end repair –
- 1. Preparation – The nerve ends are prepared to get visible ends with necrotic tissue being removed with blades leaving two normal looking ends. Flexing the joint above the nerve injury and bone shortening can be given more length if this is required.
- 2. Approximation – The nerve ends are mobilized and brought together leaving a minimal gap by applying appropriate tension. Tensionless repairs have shown to have better outcomes. During the approximation the nerve ends can be mobilised but extensive intrafasicular dissection should be avoided.
- 3. Alignment – Bloods vessels must be aligned and proper rotational alignment undertaken.
- 4. Maintenance – The nerve repair is maintained by stitches into the epineurium, commonly 9-0 or 10-0 non-absorbable sutures. Hence, it is the epineural repair that keeps the repair together. The sutures need to be placed to avoid malrotation of the nerve ends.
- C. Postoperative care
- - Immobilization for 10-14 days.
- - After this period full passive and active range of motion is initiated for rehabilitation.
- - Patients should be monitored clinically to check that nerve recovery is occurring at the expected rate. Tinel’s sign is useful in monitoring axon regeneration and should advance at about 1 mm/day. If the event of nerve recovery is not progressing, then re-exploration of the nerve may be justified.
- D. Other techniques of nerve repair
- - Nerve Grafting
What is Tinel’s sign?
Percussion over the site of a nerve injury or nerve repair elicits a tingling or electric shock like sensation along the distribution of that nerve. An advancing Tinel’s sign after nerve repair implies successful nerve regeneration towards the target organ.
Grading of muscle weakness by Medical Research Council (MRC)?
- Grade 0: No contraction or muscle movement.
- Grade 1: Trace of contraction, but no movement at the joint.
- Grade 2: Movement at the joint with gravity eliminated.
- Grade 3: Movement against gravity, but not against added resistance.
- Grade 4: Movement against external resistance with less strength than usual.
- Grade 5: Normal strength.