Neurosurgery

1. NERVE COMPESSION SYNDROMES (MBCHB LECTURES)
PROF. NIMROD J M MWANG’OMBE
MBCHB, MMED (SURG), PHD (LOND)
PROFESSOR OF SURGERY, CONSULTANT NEUROSURGEON
DEPARTMENT OF GENERAL SURGERY, SCHOOL OF MEDICINE
KENYATTA UNIVERSITY, NAIROBI KENYA.

2. Learning objectives
At the end of this presentation one should be able to appreciate the
following
1. The common nerve compression syndromes of the upper limb,
management and indications for surgery.
2. The nerve compression syndromes of the posterior fossa,
management .indications for surgery

3. Abstract
Entrapment neuropathies such as carpal tunnel
syndrome, radiculopathies, or radicular pain are the most
common peripheral neuropathies and also the most
common cause for neuropathic pain. Despite their high
prevalence, they often remain challenging to
diagnose and manage in a clinical setting. Summarising
the evidence from both preclinical and clinical studies, this
review provides an update on the aetiology and
pathophysiology of entrapment neuropathies. Potential
mechanisms are put in perspective with
clinical findings. The contemporary assessment is
discussed and diagnostic pitfalls highlighted. The
evidence for the noninvasive
and surgical management of common entrapment
neuropathies is summarised and future areas of research
are identified.
Keywords: Entrapment neuropathies, Compression
neuropathies, Carpal tunnel syndrome, Sciatica,
Radiculopathy, Radicular pain, Pathomechanisms,
Assessment, Diagnosis, Management, Treatment.

4. 1. Neuropathic Pain 2. Inflammatory pain 3. visceral pain
Neuropathic pain
• This arises from damage to neurones either peripheral or central (via
compression, ischaemia/hemorrhage, chemical or transection).
Peripheral damage results in the accumulation of abnormal sodium
and calcium channels at the site of injury. There is gene expression
alteration in number and character of receptors. Damaged neurones
discharge spontaneously and there is cross-talk to normal fibers and
recruitment of silent nociceptors.
ThreeTypes of Pain (Review)

5. • Excessive or absent discharge from primary afferents within the
dorsal horn results in overall excitation and alteration in expression of
neurotransmitter N-methyl-D-Aspartate (NMDA) receptors and
functional loss of opioid and gabaminergic systems. There is resultant
hyperexcitation with increased receptive fields, primary and
secondary hyperalgesia, and allodynia.
Higher centers undergo re-mapping and alteration, resulting in
increased excitation of afferent and cingulate cortices.
Types of Pain (cont)

6. A. INTRODUCTION
Entrapment neuropathies are caused by compression and/or irritation of peripheral
nerves as they travel through narrow anatomical spaces.
The most common entrapment neuropathy is carpal tunnel syndrome (CTS) with a
lifetime risk of 10%, which increases to a staggering 84% in patients with diabetes.
The second most common entrapment neuropathy is cubital tunnel syndrome.
Another common condition is “sciatica,” with reported prevalence values ranging
from 1.6% to 43%. The striking variation in prevalence has been attributed to the
varying definitions of “sciatica.” “sciatica” may include somatic referred pain,
radicular pain (pain evoked by ectopic discharges from a dorsal root or its ganglion),
and radiculopathy (conduction block along a spinal nerve or its roots manifesting
clinically with dermatomal sensory loss, myotomal weakness, or reflex changes).

7. Aetiology
The aetiology of entrapment neuropathies remains largely unknown.
They share several risk factors across conditions, such as increased
body mass index, occupational or physical factors, and predisposing
systemic diseases such as diabetes or hypothyroidism. Recently, genetic
predisposition is emerging as one of the strongest risk factors for
entrapment neuropathies. In addition to rare variants, genome-wide
association studies have identified several genetic susceptibility loci for
entrapment neuropathies. Many of the genes are related to connective
tissue and extracellular matrix architecture. It currently remains unclear
whether these genes increase vulnerability by altering the nerve itself
(as a substantial proportion consists of connective tissue) or the
environment through which the nerve travels (eg, the tunnels).

8. B. Pathophysiology
Our understanding of neuropathic pain is largely based on preclinical
models involving acute and severe nerve injuries.
However, human entrapment neuropathies are quite distinct from
these preclinical models because their onset is mostly slow, and the
neural injury is often of mild but chronic nature.

9. 1. Ischaemia, oedema, and intraneural
fibrosis
Intraneural ischaemia is typical of mild entrapment neuropathies.
Animal models demonstrate that extraneural pressures as low as 20 to
30 mm Hg disrupt intraneural venous circulation. These pressures are
often reached in patients with entrapment neuropathies. The ensuing
reversal of the pressure gradient necessary to assure adequate blood
supply could explain the sometimes intermittent paraesthesia, which
occur at night, in static positions.

10. 2. Demyelination and axon degeneration
Prolonged ischaemia and mechanical compromise may induce
downstream effects such as demyelination and eventually axon
degeneration. Focal demyelination is a hallmark of entrapment
neuropathies.

11. 3. Neuroinflammation
There is a wealth of preclinical data confirming an important role of
neuroinflammation in the generation and maintenance of neuropathic pain.
Neuroinflammation is characterised by activation of immune cells (eg,
macrophages and T-lymphocytes) at the site of damaged axons. Immune
cells release inflammatory mediators (eg, cytokines, chemokines, and lipid
mediators), which induce a breakdown of the blood–nerve barrier resulting
in further immune cell influx and swelling. Importantly, neuroinflammation
sensitises injured and uninjured axons and nociceptors in target tissue,
contributing to neuropathic pain initiation and maintenance. Whereas most
evidence for a link between neuroinflammation and neuropathic pain stems
from acute and severe nerve injury models, there is a growing body of
evidence suggesting that neuroinflammation is also a feature of mild chronic
nerve compression.

12. 4. Changes to axonal transport
Peripheral nerve compression and inflammation impair retrograde and
anterograde axonal transport. Its blockage can result in increased nerve
mechanosensitivity presumably by the accumulation and insertion of
ion channels at the lesion site and may contribute to symptoms in
patients with entrapment neuropathies.

13. 5. Central nervous system contributions
Because the peripheral and central nervous system form a functional
entity, injuries of peripheral nerves inevitably initiate central changes.
Clinical hallmarks of central mechanisms including bilateral sensory
deficits in unilateral painful entrapment neuropathies, widespread
hypersensitivity and impaired conditioned pain modulation have been
described in patients with entrapment neuropathies.
Clinically, such cortical changes may manifest in an impairment in
left/right judgement tasks such as found in patients with CTS.

14. 6. Psychosocial factors
Psychosocial factors often play a role as risk factors for the
development or persistence of pain.
Entrapment neuropathies can have strong psychosocial consequences
as apparent in lumbar radicular pain affecting many aspects of life,
including psychological status.

15. C. Clinical presentation
Loss of function due to reduced action potential conduction caused by
the nerve lesion.
Neuropathic pain.

16. D. Assessment
Neuropathic pain grading system
The Neuropathic Pain Special Interest Group of the International Association of the
Study of Pain introduced a grading system to assist clinicians and researchers
determining the certainty of neuropathic pain. The level of “probable” neuropathic
pain is suggested to be sufficient to initiate pharmacological treatment for
neuropathic pain. The application of the grading system may, however, be
problematic in patients with entrapment neuropathies because symptoms often
spread beyond the affected dermatome or innervation territories of the affected
nerve, patients may have very subtle sensory loss that may not be identified with
bedside sensory testing and/or patients may present with mainly gain of function,
and diagnostic tests may not be indicated (eg, skin biopsies) or may be negative
(see imaging and nerve conduction studies below). It therefore often remains
unclear whether patients with entrapment neuropathies should receive
management according to the neuropathic pain guidelines.

17. Neuropathic pain grading system

18. Clinical assessment
• The examination includes subjective assessment and localisation and
distribution of symptoms on a body chart as well as their quality, intensity,
and behaviour over 24hours.
• The medical history on potential mechanisms of injury or causes leading to
pain or neurological lesions and disorder progression.
• Important information on psychological or behavioural factors, social and
economic factors as well as occupational factors that may contribute to the
presentation.
• The physical examination: assessment of both musculoskeletal and related
neural tissue, neurological examination of sensory and motor function to
ascertain the presence of a nerve lesion.

19. Neurological examination
• Motor function assessment comprises the examination of reflex
responses and muscle strength testing.
• Sensory examination includes the assessment of large and small
sensory fibres because both can be affected in patients with nerve
entrapment.
• Provocation tests are designed to detect nerve mechanosensitivity:
Tinel sign or Phalen test for CTS, Spurling test for cervical
radiculopathy, the straight leg raise test for the lower limb.

20. Bedside sensory testing tools.
various tools for bedside sensory testing
that assess loss and gain of function in
distinct sensory fibre populations.

21. Imaging and nerve conduction studies
• MRI, ultrasound, or nerve conduction studies, Ultrasonography

22. Natural history
CTS patients who have not received treatment over an average of 2;
years20% deteriorate, 30% remain stable, and 50% show symptom
recovery.
A similar pattern presents in patients with “sciatica,” however, at least
one-third will develop persistent pain and disability

23. Management
• Conservative treatment before invasive options.
• Physiotherapy/occupational therapy for carpal tunnel syndrome: for
mild to moderate CTS, therapy usually includes advice, splinting (at
night), electrophysiological agents as well as manual therapy and/or
exercises.
• Physiotherapy is recommended as the first-line treatment for
• patients with “sciatica.”

24. Pharmacological interventions
• Oral medications do not seem to be beneficial in patients with CTS, with
nonsteroidal anti-inflammatories, diuretics, or vitamin B6 not being
superior to placebo.
• Local steroid injections seem to have a short-term benefit only, which
exceeds the effect of orally taken steroids.
• Similar results are reported by several meta-analyses for patients with
“sciatica,” suggesting that nonsteroidal anti-inflammatories, oral
corticosteroids, Tumour necrosis factor blockers, opioids, and specific
neuropathic pain medications (eg, anticonvulsants and antidepressants) do
not provide better symptom relief than placebo. Corticosteroid injections
seem to provide a small benefit in the short but not long tem.

25. Surgery for carpal tunnel syndrome
• Carpal tunnel decompression is the most common upper-limb surgery
• The 2 surgical approaches used are endoscopic and open carpal tunnel
release, with no strong evidence indicating one technique to be more
superior.
• 25% of patients do not benefit
• Potential complications include scar tenderness, persistent symptoms,
neurovascular injury, wound complication, and reduced grip strength.
• Indications for surgical consultation include moderate-to-severe or
deteriorating symptoms, daily symptoms, frequent night waking, persistent
symptoms causing functional impairment, not responding to nonsurgical
treatments and patients’ preference.

26. Carpal tunnel syndrome

27. •
Idiopathic carpal tunnel syndrome (CTS) is a common complaint,
reflecting entrapment neuropathy of the upper extremity. CTS produces
symptoms similar to those of other conditions, such as cervical
spondylosis or ischemic or neoplastic intracranial disease. Because of
these overlaps, patients with CTS are often referred to a neurosurgeon.
Optimal diagnostic criteria for this disease are still undetermined, its
diagnosis is based on the patient’s history and physical examination,
which should be confirmed by nerve conduction studies and imaging
modalities such as magnetic resonance imaging and ultrasonography.
Treatment methods include observation, medication, splinting, steroid
injections, and surgical intervention. Understanding the clinical features
and pathogenesis of CTS, as well as the therapeutic options available to
treat it, is important for neurosurgeons if they are to provide the correct
management of patients with this disease.

28. Neurol Med Chir (Tokyo) 57, 172–183, 2017
• Importance of Recognizing Carpal Tunnel Syndrome for Neurosurgeons: A Review Masatoshi
Yunoki, 1 Takahiro Kanda, 1 Kenta Suzuki, 1 Atsuhito Uneda, 1 Koji Hirashita, 1 and Kimihiro
Yoshino1 1 Department of Neurosurgery, Kagawa Rosai Hospital, Marugame, Kagawa, Japan
Abstract Idiopathic carpal tunnel syndrome (CTS) is a common complaint, reflecting entrapment
neuropathy of the upper extremity. CTS produces symptoms similar to those of other conditions,
such as cervical spondylosis or ischemic or neoplastic intracranial disease. Because of these
overlaps, patients with CTS are often referred to a neurosurgeon. Surgical treatment of CTS was
started recently in our department. Through this experience, we realized that neurosurgeons
should have an increased awareness of this condition so they can knowledgeably assess patients
with a differential diagnosis that includes CTS and cervical spinal and cerebral disease. We
conducted a literature review to gain the information needed to summarize current knowledge on
the clinical, pathogenetic, and therapeutic aspects of CTS. Because the optimal diagnostic criteria
for this disease are still undetermined, its diagnosis is based on the patient’s history and physical
examination, which should be confirmed by nerve conduction studies and imaging modalities
such as magnetic resonance imaging and ultrasonography. Treatment methods include
observation, medication, splinting, steroid injections, and surgical intervention. Understanding
the clinical features and pathogenesis of CTS, as well as the therapeutic options available to treat
it, is important for neurosurgeons if they are to provide the correct management of patients with
this disease. Key words: carpal tunnel syndrome, diagnosis, treatment, neurosurgeon

29. The carpal tunnel is a narrow channel about 1 inch long between the wrist and the hand covered by a thick band of
connective tisue on the front (palm side) of the wrist, and contains tendons and the median nerve.
Carpal tunnel syndrome occurs when the median nerve, which runs from the forearm to the palm of the hand, is compressed
by swelling of other tissues within the carpal tunnel or by narrowing of the carpal tunnel.
Themedian nerve provides sensation to the thumb, the index finger, the middle finger, and half of the ring finger and is
responsible for movement of all of the fingers and the wrist.
Symptoms of Carpal Tunnel Syndrome Common symptoms of carpal tunnel syndrome are a gradual onset of numbness or
tingling in the thumb and the index,middle, and half of the ring finger, and thumb weakness.
If left untreated, patients can develop permanent numbness in these areas of the hand and a decrease in size (atrophy) of
the thumb muscle with permanent weakness.
Carpal tunnel syndrome is a common condition that occurs more frequently in individuals who are female, middle aged, or
pregnant or have medical conditions such as diabetes, obesity, and hypothyroidism.
Certain jobs are associated with higher rates of carpal tunnel syndrome, including those involving repetitive wrist and fingers
movements (such as computer use for more than 4 hours per day) or operation of heavy machinery that applies strong
vibrations to the hands or requires forceful hand gripping.
The diagnosis of carpal tunnel syndrome is generally based on characteristic symptoms and physical examination findings,
including decreased sensation in the thumb and the index, middle, and half of the ring finger, and thumb weakness. Nerve
conduction studies and electromyography, which are specialized tests that measure nerve and muscle function, may be
performed to confirm the diagnosis of carpal tunnel syndrome. Ultrasound imaging is also a useful noninvasive test to
diagnose carpal tunnel syndrome.
Initial treatment of carpal tunnel syndrome involves avoidance of symptom-provoking activities and use of a wrist splint at
night. In addition, specialized range-of-motion wrist exercises can improve symptoms.
Steroid injection into the affected area may result in modest relief of symptoms; however, the benefit generally lasts only 1 to
3 months, and there is a small risk of worsening of nerve compression, unintentional injection into the median nerve, or
damage to tendons within the carpal tunnel.
Patients with carpal tunnel syndrome who have symptoms that do not improve after 6 weeks of nonoperative treatment or
who have symptoms of constant numbness or atrophy of the thumb muscle should be evaluated by a surgeon. In most
appropriately selected patients, surgery improves symptoms of carpal tunnel syndrome. Potential rare complications of
carpal tunnel surgery include infection, development of a painful scar, or injury to the median nerve.

30. Cubital tunnel syndrome
• Cubital tunnel syndrome is the second most common peripheral
nerve entrapment syndrome in the human body. It is the cause of
considerable pain and disability for patients. When appropriately
diagnosed, this condition may be treated by both conservative and
operative means.

31. THE ANATOMY OF THE ULNAR NERVE AND
THE CUBITAL TUNNEL
• The cubital tunnel is formed by the cubital tunnel retinaculum which
straddles a gap of about 4 mm between the medial epicondyle and the
olecranon. The floor of the tunnel is formed by the capsule and the
posterior band of the medial collateral ligament of the elbow joint. It
contains several structures, the most important of which is the ulnar nerve.
• The ulnar nerve is the terminal branch of the medial cord of the brachial
plexus, and contains fibres from the C8 and T1 spinal nerve roots. It
descends the arm just anterior to the medial intermuscular septum and
later pierces this septum in the final third of its length. Progressing
underneath the septum and adjacent to the triceps muscle, it traverses the
cubital tunnel to enter the forearm where it passes between the two heads
of the flexor carpi ulnaris muscle.

32. Symptoms and signs
Patients with ulnar nerve compression at any level have altered sensation in the
little and ring fingers, clumsiness in the hand, as the ulnar nerve is the principal
motor supply to the intrinsic muscles of the hand. In well-established cases, there
may be marked wasting of the small muscles of the hand and the ulnar-sided
muscles of the forearm.
Look for Froment’s sign, overt clawing of the ulnar-innervated digits (usually the
little and ring fingers) and abduction of the little fingers (Wartenberg’s sign).
Inspection of the elbow in extension may show a valgus deformity, possibly
secondary to a previous fracture around the elbow. Malunion after supracondylar
fracture of the humerus can result in an adult cubitus valgus deformity, which in
turn predisposes to a ulnar nerve palsy.
Tinel’s sign should be positive over the cubital tunnel itself, although some
surgeons find it easier to elicit Tinel’s sign ove the medial side of the humerus.

33. Treatment. Surgery.

34. Surgery for “sciatica”
• Lumbar microdiscectomy is the most common type of surgery
performed to relieve nerve root irritation or compression due to a
herniated disk.
• Approximately 5% of patients are worse after surgery.
• Reoperation rates of approximately 10% within 4 years.
• Conservative management should remain the first-line treatment.
• Surgery is indicated in the presence of severe or progressive
neurological deficits or persistent symptoms that are unresponsive to
conservative treatment.

35. Baldauf J, Rosenstengel C, Schroeder HWS: Nerve
compression syndromes in the posterior cranial fossa—
diagnosis and treatment. Dtsch Arztebl Int 2019; 116:
54–60. DOI: 10.3238/arztebl.2019.0054
Summary
Nerve compression syndromes in the posterior cranial
fossa can severely impair patients’ quality of life.
These syndromes are caused by compression of a cranial
nerve by an artery or vein at the zone of the nerve’s entry
to or exit from the brainstem.
The best-known neurovascular compression syndrome is
trigeminal neuralgia, followed by hemifacial spasm.
The initial treatment of trigeminal
neuralgia is medical: the first line of treatment is with
sodium-blocking anticonvulsants, such as carbamazepine.
For patients with hemifacial spasm, botulinum
toxin injection is the recommended initial treatment and
often leads to a satisfactory regression of the spasms.
If these treatments fail, a microvascular decompression
operation is indicated.
The aim of the procedure is to separate the irritating
vessel from the nerve and to keep these structures apart
permanently..
This is a causally directed form of treatment
that generally yields very good results.

36. • Tic douloureux; paroxysmal one sided facial pain, triggered by sensory
stimuli in distribution of trigeminal nerve branches. Distinguish from
other types of facial pain referred to as “atypical facial pain.” Status
trigeminus; continous facil pain/spasms.
• Epidemiology: uncommon in Africans. 4/100,000 in Western World.
Spontaneous remission for weeks/months. 2% of patients with
multiple sclerosis (MS) have trigeminal neuralgia and 18% of patients
with bilateral trigeminal neuralgia have MS
TRIGEMINAL NEURALGIA

37. • Medical therapy:
1. carbamazepine (Tegretol). 100 mg bid upto 1200 mg tid.
Drowziness. Relative leucopenia (don’t discontinue).
2. baclofen (Lioresal). 2nd drug of choice. Teratogenic. Avoid abrupt
withdrawl-hallucinations, seizures. May be combined with low dose
carbamazepine. 5mg tid, upto 20mg qid.
3. garbapentin(Neurontin)
Trigeminal neuralgia
(cont)

38. • 1. Microvascular decompression: recommended for
patients <65 years with no medical or surgical risk factors.
Failure rate 20-25%. An artery is dissected and held away
from the trigeminal nerve through a sub-occipital exposure.
• 2. Percutaneous procedures. A needle is passed under
fluoroscopic control through the foramen ovale into the
trigeminal ganglion and a radiofrequency current is passed
until a pin prick is felt as light touch over the appropriate area
of the face. Relief immediate.
• 3. Radiosurgery: a high dose of radiation is precisely aimed at
the proximal few millimeters of the trigeminal nerve as it
exits the brain stem. Pain relief may take as long as 2-6
months to appear. Elderly and frail
Surgery.

39. THANK YOU
(WESU ROCK,
TAITA-TAVETA
COUNTY)