Cn disorders and their treatments

1. CN disorder, nerve root, nerve plexuses
and peripheral nerve lesions
for
Year III PHYSIOTHERAPY
Dr alehegn Y

2. Outline
 CN disorder
 Poly-radiculopathy
 Diabetic neuropathy
 References

3. Introduction
The cranial nerves
 consist of 12 paired nerves
 that mediate variable
combinations of motor,
sensory, and autonomic
functions

4. FACIAL PAIN OR NUMBNESS
ANATOMIC CONSIDERATIONS
 The trigeminal (fifth cranial) nerve supplies sensation to the
skin of the face, anterior half of the head, and the nasal and
oral mucosa
 motor part innervates the muscles of
 chewing (including masseters and pterygoids)
 the anterior belly of the digastric, mylohyoid, tensor veli
palatini, and the tensor tympani (hearing especially for
high-pitched tones).

5. The trigeminal nerve and its branches and
sensory distribution on the face. The three
major sensory divisions of the trigeminal nerve
consist of the ophthalmic, maxillary, and
mandibular nerves

6. 1. TRIGEMINAL NEURALGIA(TN)
(TIC DOULOUREUX
 is relatively common
 annual incidence of 4–8 per 100,000 individuals.
 Age =Middle-aged and elderly persons are affected
primarily
 Sex ∼60% of cases occur in women
 Onset is typically sudden, and
 bouts tend to persist for weeks or months before
remitting spontaneously. Remissions may be long-lasting,
but in most patients, the disorder ultimately recurs.

7. TN….
ETIOLOGY AND PATHOGENESIS —
 compression of the trigeminal nerve root
 Most ccommon cause
 usually within a few millimeters of entry into the pons
(the root entry zone) .
 80 to 90 % Compression by an aberrant loop of an artery or
vein

9.  Classification — In the International Classification of Headache
Disorders, 3rd edition (ICHD-3), TN is divided into
1. Classic (or classical) trigeminal neuralgia caused by neurovascular
compression or Idiopathic TN
2. Painful trigeminal neuropathy is caused by lesions other than vascular
compression [1].
 nerve compression include vestibular schwannoma (acoustic neuroma),
meningioma, epidermoid or other cyst, or, rarely, a saccular aneurysm or
arteriovenous malformation
 Painful trigeminal neuropathy attributed to acute herpes zoster
 Postherpetic trigeminal neuropathy
 Painful posttraumatic trigeminal neuropathy
 Painful trigeminal neuropathy attributed to multiple sclerosis
plaque
 Painful trigeminal neuropathy attributed to space-occupying lesion
 Painful trigeminal neuropathy attributed to other disorder

10. TRIGEMINAL NEURALGIA…
Clinical Manifestations
 characterized by suddenexcruciating (intense, sharp,
or stabbing pain ) paroxysms of pain,
 Location/distribution : usually unilateral, superficial,
one or more branches of the fifth cranial (trigeminal)
nerve : in the lips, gums, cheek, or chin and, very
rarely, in the distribution of the ophthalmic division
of the fifth nerve.
 Duration: seldom lasts more than a few seconds or a
minute or two but may be so intense that the patient
winces, hence the term tic.
 Frequency: The paroxysms, experienced as single
jabs or clusters, tend to recur frequently, both day
and night, for several weeks at a time.
 Onset: spontaneously or movements of affected
areas by speaking, chewing, or smiling.

12. Clinical Manifestations
 the presence of trigger& trigger zones: the face, lips, or
tongue, that provoke attacks; patients may report that tactile
stimuli—e.g., washing the face, brushing the teeth, or
exposure to a draft of air—generate excruciating pain.
 An essential feature of trigeminal neuralgia is that objective
signs of sensory loss cannot be demonstrated on
examination

13. Laboratory Evaluation
 if indicated : ESR or CRP (temporalarteritis is
suspected).
 neuroimaging studies are usually
unnecessary
 indication:in patients younger than 40
years or when symptoms are bilateral or
in assessing overlying vascular lesions in
order to plan for decompression surgery.

15. TREATMENT
Trigeminal Neuralgia
Medical Rx
 Carbamazepinep-first line
 is effective in ∼50–75% of patients.
 Carbamazepine should be started as a single daily dose of 100
mg taken with food
 increased gradually (by 100 mg daily in divided doses every 1–
2 days) until substantial (>50%) pain relief is achieved.
 Most patients require a maintenance dose of 200 mg four
times daily.
 Doses >1200 mg daily provide no additional
 Duration:If treatment is effective, it is usually continued for 1
month and then tapered as tolerated
 Oxcarbazepine: if not respond to or tolerate carbamazepine
 Alternatively: 'Baclofen, lamotrigine
Surgical :
 If drug treatment fails
 most widely used method microvascular decompression to
relieve pressure on the trigeminal nerve as it exits the pons

16. BELL’S PALSY
 The most common form of facial paralysis
is Bell’s palsy.
 incidence of this idiopathic disorder
 ∼25 per 100,000 annually, or
 about 1 in 60 persons in a lifetime.
 Risk factors include pregnancy and
diabetes mellitus

18. Clinical Manifestations
 fairly abrupt, unilateral facial paralysis with maximal
weakness being attained by 48 h as a general rule.
 Common findings include the eyebrow sagging,
inability to close the eye, disappearance of the
nasolabial fold, and drooping at the affected corner
of the mouth, which is drawn to the unaffected side
 Pain behind the ear may precede the paralysis for a
day or two.
 Taste sensation may be lost unilaterally, and
hyperacusis may be present. In some cases, there is
mild cerebrospinal fluid lymphocytosis.
 Approximately 80% of patients recover within a few
weeks or months
 Recurrences are reported in ∼7% of cases
 Dx= clinically

21. The diagnosis of Bell's palsy is based upon the following criteria:
 There is a diffuse facial nerve involvement manifested by
1. paralysis of the facial muscles,
2. with or without loss of taste on the anterior two-
thirds of the tongue or
3. altered secretion of the lacrimal and salivary
glands.
 Onset is acute, over a day or two;
 the course is progressive, reaching maximal clinical
weakness/paralysis within three weeks or less from the first
day of visible weakness; and recovery or some degree of
function is present within six months.

22. DIFFERENTIAL DIAGNOSIS —
 Facial nerve palsy may be caused
 herpes zoster infection,
 Guillain-Barré syndrome,
 Otitis media, Lyme disease (neuroborreliosis),
HIV infection, and others

23. TREATMENT
Symptomatic measures include: Eye care
1. (1) the use of paper tape to depress the upper eyelid during sleep
and prevent corneal drying,
2. artificial tears; and
3. massage of the weakened muscles.
Pharmacologic therapy
 Glucocorticoids: prednisone 60–80 mg daily during the first 5 days
and then tapered over the next 5 days PLUS
 antiviral agents: valacyclovir (1000 mg daily for 5–7 days) or
acyclovir (400 mg five times daily for 10 days)
 should preferably begin within three days of symptom onset

24. Reading assignment
 MULTIPLE CRANIAL NERVE PALSIES

25. Polyradiculopathy
 A radiculopathy is a pathologic process affecting the nerve root with
clinical manifestations that may include pain, motor and sensory
symptoms, and reflex change.
 Polyradiculopathy: refers to damage to multiple nerve roots sufficient to
produce neurologic symptoms and signs such as pain, weakness, and
sensory loss
 SPINAL LEVEL — The main feature that distinguishes radiculopathy from
other neurologic disorders is that the symptoms and signs of
radiculopathy follow sensory and motor nerve root distributions
Types:
 Cervical polyradiculopathy
 Thoracic polyradiculopathy
 Lumbosacral polyradiculopathy
 The cauda equina syndrome

26. Cervical polyradiculopathy:
 presents with neck pain radiating unilaterally or bilaterally
into the arms with associated paresthesia, weakness, and
sensory loss.
Thoracic polyradiculopathy:
 is the least common of the polyradiculopathies; symptoms
include pain and paresthesia in the chest and abdomen and,
occasionally, abdominal wall weakness with herniation of
abdominal contents.

27. Lumbosacral polyradiculopathy
 accounts for the majority of polyradiculopathy cases. Central
canal spinal stenosis in this region classically presents as
neurogenic claudication, characterized by an aching that begins in
the buttocks and descends into the knees, is brought on by walking
or exercise, and is relieved by forward flexion.
The cauda equina syndrome:
 a variant of lumbosacral polyradiculopathy, is characterized by
progressive lower extremity weakness, sphincter dysfunction,
and saddle anesthesia

28. Cervical polyradiculopathy:
PATHOPHYSIOLOGY :
 causes of radiculopathy
 compressive vs nondegenerative etiologies.
 compressive radiculopathy
 The majority of radiculopathies arise from nerve root
compression .
 The two predominant mechanisms of compressive cervical
radiculopathy are
 cervical spondylosis and
 disc herniation

29. Cervical spondylosis :
 a general term for nonspecific, degenerative changes of the spine.
 Often cervical spondylosis is a cause of cervical canal stenosis, but the
two terms are not interchangeable.
 causes /risk factor
 causes of spondylosis have not been well defined,
 aging is clearly an important factor.
 Degenerative changes occur in the vertebral discs, the zygapophyseal
and uncovertebral joints, and the vertebral bodies .
 Gradually, there is bone formation in these areas, which is called
osteophyte or "hard disc."

30. Disc herniation —
 Disc herniation is most likely to result in root
compression and radicular symptoms if it occurs
laterally,
 whereas spinal cord compression and clinical
myelopathy can occur if there is herniation of a large
midline disc.

31. Nondegenerative causes
 infectious processes (especially herpes zoster and Lyme disease), nerve
root infarction, root avulsion, infiltration by tumor, infiltration by
granulomatous tissue, and demyelination
 In general, nondegenerative radiculopathies tend to affect the ventral
and dorsal root more diffusely than compressive etiologies.
 In contrast to most compressive types, nondegenerative
radiculopathies may also affect the dorsal root ganglion.
 The deficit associated with nondegenerative radiculopathy may span
multiple myotomes and dermatomes, leading to motor and sensory
deficits that are more complete than are typical for a compressive
radiculopathy

32. Cervical radiculopathy….
EPIDEMIOLOGY —
 Cervical radiculopathy is a common cause of both
acute and chronic neck pain and upper limb motor and
sensory symptoms.
 Lower cervical roots, particularly C7, are more
frequently affected by compression than higher
cervical roots

33. Cervical radiculopathy….
CLINICAL FEATURES
 neck, shoulder or arm pain, muscle weakness, sensory symptoms, or
diminished deep tendon reflexes, either alone or in combination .
 The clinical features vary by cervical nerve root involvement .
 Onset of symptoms is most frequently acute when caused by a
herniated nucleus pulposus, but may be more indolent when due to
spondylosis.
 Pain in the neck or arm occurs in nearly all patients with cervical
radiculopathy, but it is usually not of localizing value.
 Pain may be in the cervical region, the upper limb, the shoulder, or the
interscapular region. The pain may be atypical and present as chest
pain (pseudo-angina), breast pain, or facial pain .
 Sensory loss in radiculopathy is frequently mild or absent; this
seeming paradox is explained by the extensive overlap of dermatomes,

34.  Danger signs — A number of findings may point to cervical myelopathy or suggest
noncompressive etiologies for cervical radiculopathy
 Lhermitte's phenomenon, a shock-like paresthesia occurring with neck flexion,
may be present if there is compression of the cervical cord by a midline disc
herniation or spondylosis, but it may also suggest intramedullary pathology, such as
a multiple sclerosis plaque.
 Although there is no specific presentation of cervical myelopathy, symptoms often
begin with an insidious onset of gait disturbance. Other common symptoms include
sensory loss, and weakness and muscle atrophy in the hands, along with neck and
arm pain. The examination usually reveals other myelopathic features.
 A history of fever, chills, unexplained weight loss, immunosuppression, cancer, or
intravenous drug use should raise suspicion for tumor or infection as the cause of
the radiculopathy.

35. Antecedent events
 physical exertion or trauma immediately preceding
symptom onset .
 Playing golf,
 shoveling snow, and
 diving from a board
 However, most cases have no readily identifiable
precipitant

40. PHYSICAL EXAMINATION
 in patients with suspected cervical radiculopathy look for evidence of
 weakness and sensory disturbance in myotomal and dermatomal patterns.
 signs of superimposed spinal cord dysfunction (ie, myelopathy), since cervical
spondylosis may cause spinal cord compression as well as nerve root compression.
DIAGNOSIS —
 Cervical radiculopathy is a clinical, and to some extent subjective, diagnosis made on the
basis of the history and clinical findings. There is no "gold standard" test to establish or
exclude the disease

42. Rx
NONSURGICAL THERAPY: two main components
 conservative therapy and
 epidural glucocorticoid injections.
Conservative therapy
 initial treatment for patients with cervical
radiculopathy who have
 nonprogressive neurologic deficits, (including dermatomal
sensory loss and myotomal weakness),
 as long as myelopathy is not suspected.
 All patients with motor weakness should be closely
followed for evidence of progression.

43. Clinical reevaluation
 should be performed after six to eight weeks of
conservative treatment, with assessment for motor
weakness and myelopathic findings in patients who have
not improved or in those who have progressive symptoms
Epidural glucocorticoid injections :
 For patients with confirmed cervical radiculopathy who
have severe or disabling pain despite a reasonable course
(six to eight weeks) of conservative therapy, and who do
not have a progressively worsening neurologic deficit use
of epidural glucocorticoid injections rather than surgery


44. Conservative therapy
 good prognosis for recovery, conservative therapies are preferred for most
patients with compressive cervical radiculopathy.
 Conservative therapy typically consists of the following modalities, alone
or in some combination
1. Oral analgesics
2. short course of oral corticosteroids
3. Avoidance of provocative activities
4. Short-term neck immobilization with a hard or soft cervical collar
and/or cervical pillow
5. Physical therapy with exercise and gradual mobilization
6. Cervical traction

45. Oral glucocorticoids
 A short course of high-dose oral glucocorticoid therapy
may be used as initial treatment for patients with
severe cervical radicular pain.
 Prednisone 60 to 80 mg/day for five days, followed by
a taper off the medication over the ensuing 5 to 14
days, is a typical regimen.

46. Exercise therapy
 Physical therapy, range-of-motion exercises,
strengthening exercises, and aerobic exercises are
frequently employed as conservative measures for
cervical radiculopathy. These treatments are unproven,
and the few controlled trials showed conflicting results

47. Epidural glucocorticoid injections —
 Patients with persistent cervical radicular pain, with or
without radiculopathy, may benefit from epidural
glucocorticoid injections, but the data are weak and
inconsistent

48. Surgery: only for patients with
 cervical radiculopathy who have cervical nerve root compression by
MRI or CT myelography at the appropriate side and level(s) and
 persistence of radicular pain despite aggressive nonsurgical therapy
for at least 6 to 12 weeks,
 as well as progressive motor weakness that impairs function regardless
of duration.
Types of surgical Rx
 Anterior cervical discectomy and fusion
 Posterior laminoforaminotomy
 Artificial disc replacement

49. SURGERY
 Indications for surgery —
 Proposed indications for surgery in patients with cervical radiculopathy are
unremitting radicular pain despite six to eight weeks of conservative treatment,
progressive motor weakness, or the presence of myelopathy
 More stringent proposed indications for surgery require the presence of all of the
following criteria :
 Symptoms and signs of cervical radiculopathy (ie, nerve root dysfunction, pain,
or both)
 Evidence of cervical nerve root compression by MRI or CT myelography at the
appropriate side and level(s) to explain the clinical symptoms and signs
 Persistence of radicular pain despite nonsurgical therapy for at least 6 to 12
weeks or progressive motor weakness that impairs function

51. Imaging studies
1. MRI
 MRI is currently the study of choice in most patients for the initial
neuroimaging evaluation of the cervical spine, unless there is a
contraindication.
 MRI generally provides superior imaging of soft tissue
structures compared with CT myelography, but less
information about bony structures. In addition, MRI may
underestimate the amount of bony abnormality.
2. CT myelography
3. Plain radiographs — Plain radiographs of the cervical spine are
rarely diagnostic in the setting of nontraumatic cervical radiculopathy,
Thus, cervical plain films are usually not indicated in the absence of
trauma .

52. Lumbosacral radiculopathy
 Lumbosacral radiculopathy is a condition in which a disease process
affects the function of one or more lumbosacral nerve roots
ANATOMY
 The lumbar spine consists of five movable lumbar vertebral
bodies,
 numbered L1 to L5 .
 The sacrum is made up of five developmentally fused vertebral
levels (S1 to S5),followed by a terminal bony prominence, the
coccyx.

53. PATHOPHYSIOLOGY AND ETIOLOGY —
 The most common etiology  nerve root compression caused by a disc
herniation or spondylosis, which is, narrowing of the intraspinal (central)
canal, the lateral recess, or the neural foramen due to degenerative arthritis
affecting the spine.
 Additional etiologies include nonskeletal causes of nerve root compression
and noncompressive mechanisms such as infection, inflammation, neoplasm,
and vascular disease., Mass lesion or malignancy, Metastasis (most common),
Epidural abscess, Intradural tumor, particularly meningioma, neurofibroma,
and ependymoma, Lymphoma, Myeloma, Root sleeve cyst, such as a Tarlov or
perineural cyst (though most are asymptomatic and found incidentally on
MRI) , Vascular, Arteriovenous malformation, Vasculitis (nerve root
infarction),Radiation-induced vascular occlusion

54.  Additional etiologies include nonskeletal causes of nerve
root compression and noncompressive mechanisms such
as infection, inflammation, neoplasm, and vascular
disease., Mass lesion or malignancy, Metastasis (most
common), Epidural abscess, Intradural tumor,
particularly meningioma, neurofibroma, and
ependymoma, Lymphoma, Myeloma, Root sleeve cyst,
such as a Tarlov or perineural cyst (though most are
asymptomatic and found incidentally on MRI) , Vascular,
Arteriovenous malformation, Vasculitis (nerve root
infarction),Radiation-induced vascular occlusion

55. Degenerative changes — Damage to spinal nerve roots
occurs as the result of degenerative change involving three
main structures, which are:
1. The intervertebral discs
2. The uncovertebral joints (cervical spine only)
3. The zygapophyseal (facet) joints

56. EPIDEMIOLOGY —
 Lumbosacral radiculopathy is one of the most common
problems seen in neurologic consultation. Although data
are limited, the estimated lifetime prevalence is
approximately 3 to 5 percent for adults, with equal
rates among men and women.

57. CLINICAL PRESENTATIONS —
 vary according the level of nerve root or roots involved.
 The most frequent are the L5 and S1 radiculopathies.
 All lumbosacral nerve roots exit the spinal canal at the
neural foramina below their respective vertebrae. As an
example, the L5 nerve roots exit via the neural foramina at
the L5/S1 disc space level. Thus, posterolateral disc
herniation of the L4/L5 disc usually compresses the L5
nerve root, while posterolateral disc herniation of the
L5/S1 disc typically compresses the S1 nerve root.

58. L1 radiculopathy
 Lumbar disc herniation at the L1 level is rare, and
thus L1 radiculopathy is uncommon.
 Symptoms on presentation generally involve pain,
paresthesia, and sensory loss in the inguinal region
 Rarely, minor hip flexion weakness is present.

60. L2/L3/L4 radiculopathy —
 There is marked overlap of the L2, L3, and L4 innervation of the anterior thigh
muscles, making it difficult to differentiate these spinal nerve root levels based on
symptoms, neurologic examination, or electrodiagnostic testing.
 Thus, these radiculopathies are generally considered as a group.
 These nerve roots are most commonly involved in older patients with symptoms of
spinal stenosis.
 Acute back pain is the most common presenting complaint, often radiating around
the anterior aspect of the thigh down into the knee and occasionally down the medial
aspect of the lower leg as far as the arch of the foot.
 On examination, there may be weakness of hip flexion, knee extension, and hip
adduction. Higher lesions may result in greater weakness of the hip flexors. Sensation
may be reduced over the anterior thigh down to the medial aspect of the lower leg.
 A reduced knee reflex is common in the presence of moderate weakness.

63. L5 radiculopathy —
 the most common radiculopathy affecting the lumbosacral spine.
 It often presents with back pain that radiates down the lateral aspect of the leg into
the foot.
 On examination, strength can be reduced in foot dorsiflexion, toe extension, foot
inversion, and foot eversion.
 Weakness of leg abduction may also be evident in severe cases due to involvement of
gluteus minimus and medius. Atrophy may be present in the extensor digitorum brevis
muscle of the foot and the tibialis anterior muscle of the lower leg. In severe cases,
there may be "tibial ridging," a condition in which the normal convexity of the anterior
compartment of the leg is lost because of atrophy, leaving a prominent sharp contour of
the medial aspect of the tibial bone.
 Sensory loss is confined to the lateral aspect of the lower leg and dorsum of the foot,
but may be obvious only when testing sharp sensation in the web space between the
first and second digits. Reflexes are generally normal, although the internal hamstring
reflex may be diminished on the symptomatic side.

65. S1 radiculopathy —
 pain radiates down the posterior aspect of the leg into the foot
from the back.
 On examination, weakness of plantar flexion (gastrocnemius
muscle) is specific.
 There may also be weakness of leg extension (gluteus maximus)
and knee flexion (biceps femoris long and short heads).
 Sensation is generally reduced on the posterior aspect of the leg
and the lateral edge of the foot. Ankle reflex loss is typical.

68. S2/S3/S4 radiculopathy —
 Structural radiculopathies at these lower levels are less
common than other lumbosacral radiculopathies, but
may be caused by a large central disc compressing the
nerve roots intrathecally at a higher level (eg, L5).
 Patients can present with sacral or buttock pain that
radiates down the posterior aspect of the leg or into the
perineum. Weakness may be minimal, with urinary and
fecal incontinence as well as sexual dysfunction.

69. Severity
 Acute lumbosacral radiculopathy can be separated into three general
categories from least to most severe:
1. Pure sensory/painful radicular pattern, characterized by radicular pain and a
segmental pattern of sensory dysfunction but no other neurologic deficits
2. Mild motor deficit pattern, characterized by radicular pain, sensory
dysfunction, and mild nonprogressive segmental motor weakness and/or reflex
change
3. Marked motor deficit pattern, characterized by radicular pain and sensory
dysfunction with severe or worsening motor deficits

70. EVALUATION AND DIAGNOSIS —
 The diagnosis of a lumbosacral radiculopathy is
clinical, and can usually be made based upon
compatible symptoms and examination findings.


71.  Urgent neuroimaging in the initial assessment for
patients with any of the following conditions
1. Acute radiculopathy with progressive neurologic
deficits
2. Radiculopathy with urinary retention, saddle
anesthesia, or bilateral neurologic symptoms or signs
3. Suspected neoplasm
4. Suspected epidural abscess

72. Maneuvers
 Specific maneuvers can be helpful in determining
whether symptoms are radicular in nature.
 These include the straight leg raise, the contralateral
straight leg raise, and the reverse straight leg raise
(also referred to as femoral stretch)

73.  The straight leg raise test is done with the patient supine. The examiner raises the
patient's extended leg on the symptomatic side with the foot dorsiflexed, being careful
that the patient is not actively "helping" in lifting the leg. Straight leg raising results in
an increase in dural tension in the low lumbar and high sacral levels.
 •Lasègue's sign is the presence or worsening of radicular pain (not just low back pain or
hamstring pain) with the straight leg maneuver (ie, hip flexion with the leg extended at
the knee). In contrast, radicular pain is absent or unchanged when the hip is flexed with
the leg in flexion at the knee. A positive Lasègue's sign usually occurs when hip flexion is
between 30 and 60 degrees, though positive tests can also occur at smaller and larger
degrees of hip flexion.
 The bowstring sign refers to the relief of radicular pain when the knee is flexed during
a positive straight leg raise.

74.  The contralateral (crossed) straight leg raise test refers to passive elevation of the
unaffected leg by the examiner. The test is positive when lifting the unaffected leg
reproduces radicular pain in the affected leg. It is relatively specific for
radiculopathy due to disc herniation, but has poor sensitivity [40,41].
 The reverse straight leg raise (femoral stretch) test is accomplished by placing the
patient prone on the table and passively extending the hip and leg straight up off
the plane of the table. This maneuver is most useful for evaluating the L2, L3, and
L4 roots. However, the value of this test is limited by inadequate information on its
sensitivity and specificity.
 Patrick's test is a maneuver during which the hip is externally rotated with the
ipsilateral knee flexed at 90 degrees and placed on the opposite knee. The test is
positive if it elicits hip or buttock pain. A positive test raises suspicion for hip or
sacroiliac disease. However, it is nonspecific for a radicular process.

75.  Neuroimaging — For imaging of the lumbar spine, MRI,
CT, and CT myelography (CT scan after intrathecal
administration of contrast media) are equally sensitive
for the diagnosis of disc herniation

76. Cerebrospinal fluid analysis —
 A lumbar puncture for cerebrospinal fluid (CSF)
evaluation is indicated if there is suspicion for a
neoplastic or infectious cause for radiculopathy and the
etiology cannot be determined by neuroimaging or
other methods (algorithm 1). However, lumbar puncture
is usually not obtained when there is suspicion for
epidural abscess

78.  The diagnosis of a lumbosacral radiculopathy is clinical, and can
usually be made based upon compatible symptoms and examination
findings.
 Immediate diagnostic testing is not necessary for patients with
suspected radiculopathy who are neurologically intact and not
suspected of having underlying neoplasm, infection, or
inflammation
 Nevertheless, testing is suggested to confirm the diagnosis and
etiology for patients who have persistent symptoms that are not
adequately controlled with conservative therapy and for whom
invasive treatment options are an option

79. DDX for lumbosacral
radiculopathy
 a herniated disc,
 lumbar spinal stenosis,
 cauda equina syndrome,
 diabetic amyotrophy,
 lumbosacral plexopathy, and
 mononeuropathies of the leg, such as femoral, sciatic,
peroneal, and tibial nerve lesions.

80. MANAGEMENT
 For patients with acute lumbosacral radiculopathy, the
objectives of treatment are to ameliorate pain
(symptomatic treatment) and to address the specific
underlying process (mechanism-specific treatment) if
necessary

81.  Neoplastic or infectious etiologies of radiculopathy
require prompt mechanism-specific treatment. Though
rare, cauda equina syndrome represents a true
surgical emergency where decompression should be
performed within 24 hours, and within 12 hours if
possible.

82.  With radiculopathy caused by disc herniation or
foraminal stenosis, symptomatic treatment is used
during the acute period.
 However, mechanism-specific treatment is indicated if
there is progressive neurologic compromise and/or
persistent symptoms that are unresponsive to time and
conservative measures.

83.  Since lumbosacral radiculopathy due to disc herniation is typically self-limited,
symptomatic treatment is used to tide the patient over the acute period. In
patients who have underlying lumbar spinal stenosis due to degenerative arthritis,
the radicular symptoms can wax and wane, although the long-term prognosis may be
less favorable than a disc herniation.
In order to reduce the risk of recurrent symptoms, a program of weight reduction should
be encouraged in patients with elevated body mass index.

 Surgery for disc herniation and lumbar spinal stenosis is most commonly performed
because of persistent symptoms or progressive neurological impairment. In the
setting of progressive neurological impairment, rapid surgical consultation should be
considered.

84. SYMPTOMATIC TREATMENT —
 Lumbosacral radiculopathy is often extremely painful.
 Analgesic medications such as nonsteroidal anti-
inflammatory drugs (NSAIDs) or acetaminophen and
activity modification are the mainstay of treatment.
 Physical therapy is often tried for patients with mild to
moderate persistent symptoms, but evidence of
effectiveness is lacking.

85.  Systemic or epidural glucocorticoids are options for patients with
acute lumbosacral radiculopathy who have persistent severe
radicular symptoms that are refractory to nonnarcotic analgesics
and activity modification. However, with either systemic or epidural
glucocorticoids, benefit, if any, is modest and transient.
 Surgery: For patients with persistent disabling lumbar radicular
symptoms who desire surgery and are good candidates, either open
discectomy or microdiscectomy are reasonable options.

 cute lumbosacral radiculopathy caused by disc herniation or
foraminal stenosis is often extremely painful, but the likelihood of
spontaneous improvement is high.

86. DIABETIC NEUROPATHY
 Most common of the chronic DM complications
 Occurs in ~50% of individuals with long-standing
type 1 & type 2 DM
 Impairs quality of life : Most important risk factor
for foot ulcer and amputation
Risk factors
 duration of DM
 glycemic control.
 obesity, hypertension, smoking , alcohol use and
dyslipidemia.

87.  Clinical evaluation for diabetic neuropathy includes
detailed history on symptoms like
 burning , tingling and pains;
 Erectile dysfunction in men;
 glycemic control;
 presence nother risk factors , and detailed neurologic exam
especially sensory,reflex and motor exam of the extremities.
 May manifest as polyneuropathy, mononeuropathy,
and/or autonomic neuropathy

88. DISTAL SYMMETRIC POLYNEUROPATHY
 Commonest type of diabetic neuropathy.
 Distal symmetric sensory or sensorimotor
neuropathy
 Pain sensation and vasculopathy ulcer risk
 Patients complain of numbness, tingling, sharpness,
or burning that begins in the feet / hands &
spreads proximally
 Pain is present at rest and worsens at night.
 Physical examination reveals
 sensory loss, loss of ankle deep-tendon reflexes, and
abnormal position sense
 It is a diagnosis of exclusion

89. AUTONOMIC NEUROPATHY
 with long-standing type 1 or 2 DM
 DM-related autonomic neuropathy can involve the cardiovascular,
gastrointestinal, genitourinary, sudomotor, and metabolic systems.
 Autonomic neuropathies affecting the cardiovascular system cause a
resting tachycardia and orthostatic hypotension. Reports of sudden death
have also been mattributed to autonomic neuropathy.
 Gastroparesis and bladderemptying abnormalities are often caused by
the autonomic neuropathy seen in DM.
 Hyperhidrosis of the upper extremities and anhidrosis of the lower
extremities result from sympathetic nervous system dysfunction.
Anhidrosis of the feet can promote dry skin with cracking, which
increases the risk of foot ulcers.
 Autonomic neuropathy may reduce counterregulatory hormone release
(especially catecholamines), leading to an inability to sense
hypoglycemia appropriatey

90. c. DIABETIC POLYRADICULOPATHY
 It is a syndrome characterized by severe disabling pain in the
distribution of one or more nerve roots. It may be accompanied
by motor weakness.
 Intercostal or truncal radiculopathy causes pain over the thorax
or abdomen.
 Involvement of the lumbar plexus or femoral nerve may cause
severe pain in the thigh or hip and may be associated with muscle
weakness in the hip flexors or extensors (diabetic amyotrophy).
 – Fortunately, diabetic polyradiculopathies are usually self-limited
and resolve over 6–12 months.

91. D. MONONEUROPATHY
 It is dysfunction of isolated cranial or peripheral Nerves.
 It is less common than polyneuropathy in DM
 It presents with pain and motor weakness in the distribution of a single nerve.
 Carpal tunnel syndrome….
 Involvement of the third cranial nerve is most common and is heralded by
diplopia. Physical examination reveals ptosis and ophthalmoplegia with normal
pupillary constriction to light.
 Sometimes other cranial nerves, such as IV, VI, or VII (Bell’s palsy), are affected.

92. TREATMENT OF DIABETIC NEUROPATHY
 Improve glycemic profile
 May use analgesics initially
 Tricyclic antidepressants – amitriptyline 25mg po nocte – may
increase dose gradually
 Carbamazepine 200mg po nocte & increased gradually
 Refer to neurologist

93. References
 Harrisson internal medicine 21th ed.
 Uptodate