Peripheral nervous system pathology - PowerPoint Presentation

Slide1

Peripheral nervous system pathology

General informations

about anatomy, physyology and pathology of the peripheral nervous system

Polineuropathies

(general features, genetic neuropathies, diabethic neuropathy, diagnosis and avaluation of the peripheral nervous system

Guillain Barre syndrome (poliradiculoneuritis)

Lumbar, sacrate and coccigeal plexus

Slide2

Slide3

Neuron

Slide4

Motor neuron: functional unit of the neuromuscular system

Consist of

Lower motor neuron (anterior horn-spinal cord; cranial nerve motor nucleus-brain stem)

Axon of that neuron

Multiple muscle

fibers it innervates

Slide5

Neuron-to-muscle-fiber ratio:

Muscles with highly refined movements (extrinsic muscles of the eye) (1:10)

Coarse and stereotyped movements (calf muscles) (1:1800)

Slide6

Transmiterea informaţiei – depolarizare, potenţial de acţiune

Canale de sodiu

Slide7

Canal de potasiu

Canal de calciu

Slide8

Sinapsele pot fi local

izate oriunde – la nivelul dendritelor (1), corpului celular (2), axonului (3) sau terminatiilor axonale (4)

S

y

naps

e

Slide9

Sinapsa

Slide10

Normal peripheral nerve

Slide11

Nerve fiber: principal structural component of peripheral nerve;

Composed of:

Axon

With its Schwann cells and myelin sheath

A nerve consists of numerous fibers that are grouped into

fascicles

Myelinated and unmyelinated nerve fibers are intermingled within the fascicle

Slide12

Three major

connective

tissue

components of peripheral nerve

Epineurium

(encloses the entire nerve)Perineurium

(encloses each fascicle)

Endoneurium

(surrounds individual nerve fibers)

Slide13

Slide14

colagen

f

ibr

ă nemielinizată

f

ibr

ă mielinizată

elastină

macrofag

capilar

neutrofil

fibroblast

mastocit

limfocit

substanţă de bază

Slide15

Peripheral axons contain organelles and cytoskeletal structures (microfilaments, neurofilaments etc)

Protein synthesis

does not

occur in the axon

Axoplasmic flow (

anterograde

) delivers proteins and other substances synthesized in the perikaryon down the axonRetrograde

transport system serves as a feedback system for the cell body.

Slide16

Myelinated

fiber in sural nerve (most commonly examined by biopsy)

2 to 16 µm in diameter

Smaller axons

Average 4 µm

Twice as numerous as the larger axons

Axons are myelinated in segments (

internodes

) separated by nodes of Ranvier

A

single

Schwann cell supplies the myelin sheath for each internode

Slide17

Unmyelinated axons

Far more numerous than myelinated axons

Range in size from 0.2 to 3 µm

Enveloped by Schwann cell

cytoplasm

(5 to 20 axons in humans)

The Schwann cells

Pale oval nuclei

Elongated bipolar cell body

Slide18

Myelin is composed of

lipids

and

proteins

Slide19

Pathology

Slide20

Two main responses of peripheral nerve to injury:

Diseases that affect primarily the Schwann cell -

segmental demyelination

Involvement of the neuron and its axon leads to

axonal degeneration

May be followed by

axonal regeneration

and

reinnervation of muscle

Two principal pathologic processes seen in skeletal muscle

Denervation atrophy

, which follows loss of axons

Myopathy

primary abnormality of the muscle fiber itself

General Reactions of the Motor Unit

Slide21

SEGMENTAL DEMYELINATION

Occurs

Dysfunction of the

Schwann cell

(as in Guillain-Barré Syndrome)

Damage to the

myelin sheath (e.g., in hereditary motor and sensory neuropathy)

Random

and

multifocal

The denuded axon provides a stimulus for

remyelination

Newly myelinated internodes are

shorter

than normal with

thin

myelin sheath

Slide22

Slide23

Onion bulbs:

Thinly myelinated axon surrounded by concentrically arranged Schwann cells

The result of

demyelination

and

remyelination

(chronic demyelinating neuropathies)

Slide24

AXONAL DEGENERATION AND MUSCLE FIBER ATROPHY

Axonal degeneration is the result of primary destruction of the axon, with secondary disintegration of its myelin sheath.

May be

Focal

(such as trauma or ischemia)

More

generalized

abnormality affecting

The neuron cell body (

neuronopathy

) or

Axon (

axonopathy

)

Slide25

Wallerian degeneration

Much more prominent after focal injury

The distal part of the axon will initially degenerate

Sprouting axonal branches from the proximal part (axonal regeneration 1mm/day)

Reestablishing contact with the muscle fibers

Slide26

With axonal degeneration there is

denervation

atrophy

of the muscle fibers within the affected motor unit

The atrophic fibers are

smaller than normal and have a roughly

triangular

shape ("

angulated

").

Rounded zone of disorganized filaments in the center of the fiber (

target fiber

) –due to cytoskeletal reorganization

Slide27

Reinnervation of atrophic muscle fiber:

From neighboring motor unit

Increased muscle fibers per motor unit

Slide28

Slide29

Peripheral nervous system

Slide30

Disorders of the Peripheral Nervous System

Slide31

Polineuropathies

Diabetic neuropathy

Evaluation of peripheral neuropathies

Poliradiculoneuritis

Lumbar and sacrate plexus

Slide32

Peripheral Neuropathy

Any disease of the peripheral nerves of any cause

Polyneuropathy – distal symmetric distribution

Mononeuropathy Multiplex – multifocal random

Mononeuropathy – single nerve involvement

Slide33

Polyneuropathy

Pathologic involvement of peripheral nerves usually due to acquired toxic and metabolic states

Manifestations:

Distribution – distal symmetrical (glove-stocking distribution)

First symptoms tend to be sensory loss or dysfunction (dysesthesias)

Signs and symptoms of lower motor neuron disease (decreased DTRs, atrophy, weakness)

Slide34

Polyneuropathy

Vary in:

Rate of disease evolution

Degree of severity

Small fiber vs. large fiber involvement

Small fiber symptoms : pain and temperature disturbances (numbness, painful paresthesias)

Large fiber symptoms and signs : weakness, areflexia, sensory ataxia or loss of position and vibration senseAxonal vs. demyelinating

Slide35

Common Causes of Polyneuropathy

Diabetes mellitus

Uremia

Vit. B deficiency

Critical illness

Hypothyroidism

CarcinomasHIV

Slide36

Common Causes of polyneuropathy

Drugs

Amiodarone

Antineoplastics (cisplatin, vincristine)

Dapsone

Hydralazine

IsoniazidPyridoxinePhenytoin

Metronidazole

Toxins

Arsenic

Diphtheria Toxin

Inorganic lead

Organophosphates

Thallium

Slide37

Clinical picture

Motor

Sensory

Trophic

Slide38

Pathogenical Classification of polyneuropathy:

d

emielin

ating

axonal

mixt (diabet

es

, alco

h

ol)

Slide39

Classification of polyneuropathy:

Axonal

Acute – relatively uncommon

Massive intoxications – arsenic

Subacute – metabolic/toxic

Chronic – 6 months- yearsHereditary neuropathies – slow course, absence of positive symptoms, mainly motor, absence of systemic disorderMost are autosomal dominant but some are also autosomal recessive

Metabolic/toxic

Slide40

Classification of polyneuropathy :

Demyelinating

Acute – Guillain-Barre Syndrome (GBS)

Subacute – all are acquired

Relapsing-remitting neuropathy (toxic)

Chronic –Hereditary

Inflammatory -CIDP

Toxic

Metabolic

Slide41

Polyneuropathies

Genetic Neuropathies

Most common is

Hereditary motor sensory neuropathy I and II

–

autosomal

dominant

peroneal

muscular atrophy

Slide42

Polyneuropathies

Acquired demyelinating

Acute : GBS – monophasic

Chronic : CIDP – slowly progressive or relapsing

May be treated with steroids, plasmapheresis and immunosuppressants

Slide43

Polyneuropathies

Diabetic Polyneuropathy

Due to long standing hyperglycemia

May take almost any form

Slide44

Polyneuropathies

Neuropathies of dysproteinemia

Multiple myeloma –especially of the osteosclerotic type

Benign monoclonal gammopathy

Infectious: Lyme disease, lepper

Neuropathies of HIV infection

Depends on the stage of the disease

GBS or CIDP- following seroconversion (asymptomatic)

Subacute to chronic mononeuritis multiplex (symptomatic)

Late symptomatic –distal symmetric sensory polyneuropathy or asymmetric painful polyradiculopathy involving the cauda equina caused by CMV

Slide45

Polyneuropathies

Autonomic neuropathies

Usually part of the more generalized polyneuropathy

Symptoms usually negative (postural hypotension, faintness, anhidrosis, hypothermia, bladder atony, obstipation, sexual impotence, dry eyes and mouth)

Positive symptoms include paroxysmal tachycardia, hypertension, diarrhea, hyperhidrosis

Slide46

Polyneuropathies

Plexopathies

Causes:

Trauma

Cervical rib band

Malignant tumor infiltration

Radiation

Idiopathic

Upper brachial plexopathy: weakness, atrophy and pain in the shoulder girdle and arm

Lower brachial plexopathy: weakness, atrophy and sensory loss or pain in the distal arm and hand

Slide47

Recovery

The PNS has an excellent ability to regenerate

2 months to years

Depends on the nature of neuropathy (axonal vs demyelinating)

Depends on whether the cause of the neuropathy has been eliminated

Slide48

Treatment

Et

h

iologic

al

S

ymptomaticpain – carbamazepine, phenitoin, gabapentin, pregabalin, triciclic antidepressants

Muscle cramps

– baclofen (Lioresal), benzodiazepine

s in small doses

Cauzalgia –alfa lipoic

acid

, eventual

ly

haloperidol, levomepromazin

Nerve trophic substances (benfothiamine, alpha lipoic acid, B vitamins)

Slide49

Mononeuritis multiplex

Simultaneous or sequential involvement of individual noncontiguous nerve trunks

Multifocal and random

1/3 demyelinating

2/3 axonal

Causes :

Vasculitis - 50% (PAN, SLE, RA, mixed CTD)

Infectious –leprosy

Granulomatous disease

Idiopathic

Slide50

Ereditary neuropathies

Slide51

Hereditary neuropathies

HMSN

I – Charcot Marie-Tooth

Most frequently encountered

. AD

Demielin

ating type of Charcot-Marie Tooth disease

Peripheral nerve hipertrophy – “onion bulbs

”

Starts between

5

and

20

years

Motor deficit is more important in lower limbs:

steppage

;

pes escavatum

.

Sensory deficits are discrete

.

Autonomic damage (cold feet and legs,

livedo reticularis,

other trophic changes, pupilary abnormalities, heart rhytm abnormalities

).

Essential tremor, OT reflexes are abolished, enlargement of peripheral nerves

As

s

oci

ated with optic atrophy

–

HMSN

t

y

p

e

VI

Associated with retinitis pigmentosa

–

HMSN

t

y

p

e

VII

Slide52

HMSN I

Slide53

Hereditary neuropathies

HMSN

II –axonal

type of CMT

AD

Debut 20-40

years old; no nerve hypertrophies.HMSN

III – Déjérine-Sottas

AD

or

AR

H

y

po- de-

and remielination

; “

onion bulb

” aspect

Starts at

1-10

years

Developpment slowing; motor distal deficits and atrophies; rapid sensory damage

(pareste

s

i

ae

);

peripheral nerve enlargement; kyphos

colio

sis

,

non

reactive

pupils and

nistagmus,

intelectual impairment

Quickly evolving

Slide54

HMSN

IV –

R

efsum

diseaseAR; first symprtoms before 20 years;Segmental demielination, “onion bulb” aspect, Retinită pigmentară, polineuropatie, ataxie cerebeloasă, hipoacuzie, ihtioză, anosmie, cardiomiopatie, tulburări ale scheletului

Dozarea acidului fitanic

Neuropatia ereditară sensibilă la presiune (neuropatia tomaculară)

AD; demielinizare segmentară; îngroşare internodală în formă de cârnat

Decadele 2-3 de viaţă, paralizii recurente de nervi periferici după compresiuni

Neuropatii ereditare senzitive şi autonome

Afectarea preferenţială a fibrelor subţiri

Hereditary neuropathies

Slide55

Slide56

Polineuropatia alcoolică

Degenerescenţă axonală (influenţa directă a alcoolului) cu demielinizare secundară (malnutriţie)

Debut insidios (săptămâni/luni); ocazional acut – zile

Tulburări simpatico-motorii, senzaţie de arsură, durere la compresiunea maselor musculare, crampe musculare, ataxia mersului, mononeuropatii

Slide57

Polineuropathies

Diabetic neuropathy

Evaluation of peripheral neuropathies

Poliradiculoneuritis

Lumbar and sacrate plexus

Slide58

Diabetic Neuropathy

About 60-70% of people with diabetes have mild to severe forms of nervous system damage,

More than 60% of nontraumatic lower-limb amputations in the United States occur among people with diabetes.

Risk Factors

Glucose control

Duration of diabetes

Damage to blood vessels

Mechanical injury to nerves

Autoimmune factors

Genetic susceptibility

Lifestyle factors – smoking, diet

Slide59

Pathogenesis of Diabetic Neuropathy

Metabolic factors

High blood glucose

Advanced glycation end products

Sorbitol

Abnormal blood fat levels

Oxydative stress

Ischemia

Nerve fiber repair mechanisms

Both axonal and demielinative pathologic processes

Slide60

Classification of Diabetic Neuropathy

Somatic neuropathy

Symmetric polyneuropathy

Polyradiculopathy

Mononeuropathy

Autonomic neuropathy

Slide61

Symmetric Polyneuropathy

Most common form of diabetic neuropathy

Affects distal lower extremities and hands (“stocking-glove” sensory loss)

Symptoms/Signs

Pain

Paresthesia/dysesthesia

Loss of vibratory sensationAmyotrophy

Slide62

Polyradiculopathy

Lumbar polyradiculopathy (diabetic amyotrophy)

Thigh pain followed by muscle weakness and atrophy

Thoracic polyradiculopathy

Severe pain on one or both sides of the abdomen, possibly in a band-like pattern

Diabetic neuropathic cachexia

Polyradiculopathy + peripheral neuropathyAssociated with weight loss and depression

Slide63

Mononeuropathy

Peripheral mononeuropathy

Single nerve damage due to compression or ischemia

Monophasic evolution

Occurs in wrist (carpal tunnel syndrome), elbow, or foot (unilateral foot drop)

Mononevritis multiplex – random involvement of several unrelated nerves

Slide64

Cranial mononeuropathy

Most frequently oculomotory nerves (

III, VI şi IV), facial

nerve

, optic

nerve

(optic anterior ischemic neuropathy)Diabetic oftalmoplegiaRareRapid evolution (1-2 days), with painful ophtalmoplegia

Mononeuropathy

Slide65

Autonomic neuropathy

Affects the autonomic nerves controlling internal organs

Peripheral

Genitourinary

Gastrointestinal

Cardiovascular

Is classified as clinical or subclinical based on the presence or absence of symptoms

Slide66

Autonomic neuropathy

Cardiovascular

y

Ta

c

hicardi

a, diminished tolerance for effort

Cardiac d

enervar

vation

Ortostat

ic hypotension

Gastrointestinal

Esophageal dysfunction

Gastropare

sis

diabetic

a

Diar

h

e

a

Constipa

tion

Incontine

nce

Urogenital

Erectile dy

sfunc

t

i

on

Retrograd e

jacul

ation

Cistopat

hy

Neurological bladder

Neurovascular

y

Intoleran

ce to heat

Gustative sudation

Dry skin

Metabolic

and

h

y

potalamic

Unnoticed

h

y

poglicemi

a

Lack of response to hypoglicemia

Autonomic dysfunction in connection to hypoglicemia

Pupilar

y

Argyll-Robertson

sign

Slide67

Treatment

Strict glycemic c

ontrol

Interven

tion on pathogenic pathways

:

Aldoz-reductase inhibitors –block the calea polyol

pathway

Alpha l

ipoic

acid

(600-800 mg/zi)

Gamma

linolenic

acid

NGF

(possibly)

Preven

ting

/

improvement of symptoms

: analge

t

ic

s

, antidepres

sants

Tryciclic antidepressants,

Gabapentin

Pregabalin

Slide68

Complications of Polyneuropathy

Ulcers

Charcot arthropathy

Dislocation and stress fractures

Amputation - Risk factors include:

Peripheral neuropathy with loss of protective sensation

Altered biomechanics (with neuropathy)Evidence of increased pressure (callus)Peripheral vascular disease

History of ulcers or amputation

Severe nail pathology

Slide69

Diabetic foot

Joint and tegumentary lesions in patients with neuropathy and/or peripheral vascular disease

40-60%

of non traumatic amputations

30-50%

of amputees will repeat the procedure for the opposite limb during the next

1-3 years.

Motor neuropathy

shape changess of foot

overcharging of pressure points

repeated microtrauma

Sensory neuropathy

lack of pain

Not using the defense mechanisms

Autonomic neuropathy

altered skin reaction mechanisms

Alter

ed skin

m

y

crocircula

tion

Ulcera

tions

Slide70

Slide71

Slide72

Polineuropathies

Diabetic neuropathy

Evaluation of peripheral neuropathies

Poliradiculoneuritis

Lumbar and sacrate plexus

Slide73

Diagnostic Tests

Clinical examination

Nerve conduction studies

Slide74

Evaluation

Calibrated tuning fork

Semmes–Weinstein Monofilament

s

Quantitative sensory testing

(

electrical, thermal, vibratory, sensory treshold

)

Slide75

Electrodiagnostics

Objective proof of lesions

Quantitative evaluation

Spreading and type of nerve damage

Slide76

Electrodiagnosis : EMG-NSS

Neurophysiologic study

Neuropathy vs. myopathy

Localization of lesion in the AHC, root, plexus, or distal nerve trunk, NMJ, muscle

Generalized polyneuropathy or multifocal neuropathy

Upper vs. lower motor neuron disease

Axonal vs. demyelinating neuropathyActivity (acute, chronic, regenerating)

If in the peripheral nerve trunk, the site of the lesion

Slide77

Electromyogram – Nerve Stimulation Studies (nerve conduction velocity)

Slide78

Nerve Biopsy

Done in the sural nerve

Indicated for : asymmetric and multifocal neuropathic disorders

In diseases characterized by nerve enlargements

In establishing the diagnosis in some genetically determined disorders

Slide79

Other tests

Genetical

Autonomic tests

(

heart rate variability

)

CSF

Slide80

Polineuropathies

Diabetic neuropathy

Evaluation of peripheral neuropathies

Poliradiculoneuritis

Lumbar and sacrate plexus

Slide81

Guillain Barre syndrome

Slide82

Guilllain Barre Syndrome (GBS)

GBS is defined as

“a

syndrome

of acute weakness of the limbs and reduced or absent reflexes, with or without sensory loss attributable to a disorder of the peripheral nerves not due to systemic disease” (Hughes. 1990).

GBS is a

clinical

diagnosis though there are frequently abnormal laboratory features including an elevated CSF protein and evidence of peripheral nerve demyelination (Hughes. 1994; Hartung et al. 1998).

Slide83

Guillain-Barre Syndrome

An acquired disease of the peripheral nervous system

Clinical:

Major features: weakness and areflexia

The most common cause of acute flaccid paralysis in all ages.

No specific test to confirm the diagnosis

A syndrome rather than a disease

Slide84

The typical illness evolves over weeks usually following an infectious disease:

1. Paresthesiaes usually hearld the disease

2. Fairly symmetric weakness in the legs, later the arms and, often, respiratory and facial muscles

3. Diminution and loss of the DTRs

4. Albuminocytologic dissociation

5. Recovery over weeks to months

Slide85

Jean-Baptiste Octave Landry

Slide86

Georges Guillain

Guillain, Barre & Strohl 1916

Revue Neurologique

Two soldiers in Amiens developing paralysis and loss of DTRs.

A new diagnostic feature: albuminocytologic dissociation in the CSF

No mention of Landry

Slide87

Guillain-barre Syndrome

Clinical features

Progressive weakness and diminished deep tendon reflexes in a symmetric distribution.

Ascending progression – most common

5 – 10% upper >> lower

5-10% proximal >> distal

Slide88

Guillain-barre Syndrome

Clinical features

Sensory disturbances: pain or paresthesias

Cranial nerves

Autonomic disturbances – infrequent but life threatening.

15-20% progress to respiratory failure.

Slide89

Clinical features

Stages:

Progression phase- days to weeks, max. 6 weeks. Period of major complications

Plateau phase - days to weeks

Recovery – weeks to months

Slide90

Laboratory findings:

CSF

normal cell count – up to 10 lymphocytes

elevated protein – 80-200 mg/dl , after 1 week

Slide91

Laboratory findings

Electrophysiological tests:

80% abnormal studies

Multiple nerves must be studied

Evidence of multifocal demyelination in motor and sensory nerves.

prolonged distal latency

Reduction of the F WAVE response and H-REFLEX.

H REFLEX – single most sensitive test for early GBS, absent in 97% of pts in the first week (Gordon at al. neurol 2001)

Slide92

Pathophysiology

Immune mediated disease

Possible mechanism: autoAB bind to glycoproteins on peripheral myelin , causing a cascade of events which eventually destroy the myelin.

Slide93

Pathology

Depend upon the form of GBS.

AIDP and MILLER-FISHER:

Inflammation and demyelination

More severe inflammation at the junction of dorsal and ventral roots at the site of the dural attachment.

Secondary axonal degeneration

Motor and motor-sensory variants:

Axonal degeneration without an inflammatory response

The immune process is directed at the nodes of Ranvier

No demyelination

Slide94

Pathophysiology

50 – 70% have an antecedent illness within the previous 4 weeks.

URTI, gastroenteritis

C. Jejuni – more severe symptoms

CMV, EBV

Immunizations:

“swine flu” vaccine (1976)

Rabies vaccine

Slide95

Infectious Systemic

Viral: Influenza, Coxsackie, EBV, Herpes, HIV, Hepatitis, CMV, WNV

Bacterial: Campylobacter jejuni, Mycoplasma, E. coli

Parasitic: Malaria, Toxoplasmosis

Hodgkins

Hyperthyroidism

Sarcoidosis

Collagen Vascular d.

Renal d.

Other events:

Surgery

Immunization

Pregnancy

Envenomization

Bone marrow transplantation

Slide96

Therapy

Supportive

Monitoring: BP, HR, RR, TEMP.

Frequent physical examinations to establish a trend.

Serial lung function testing

If dysphagia or shoulder weakness: respiratory assistance may be necessary.

Slide97

Therapy

Indications for transfer to ICU:

Respiratory failure

Autonomic dysfunction

Bulbar dysfunction

Bilateral facial weakness

aspiration

Slide98

Therapy

Corticosteroids:

First immunotherapy for GBS

“Corticosteroid medications do not seem to help improve symptoms or lessen nerve damage from Guillain-Barre syndrome” -

The Cochrane Database of Systematic Reviews 2000 (6 RCT’s, 195 pts treated with steroids vs 187 pts with supportive care)

No indication as monotherapy, evidence of benefit if added to IVIG.

Slide99

Therapy

Plasma exchange

reduce length of stay in the ICU and in hospital

Reduce need for and period of ventilation

Reduce length to unaided walking and neurological sequele.

4 double-volume exchanges on alternate days over 1 week.

exchange with albumin 5%

more beneficial when started within seven days of the disease onset.

Slide100

Therapy

IVIG

Probably same effects as plasma exchange or even superior

More available, less side effects

2 g/ Kg over 2-4 days

Caution: early transient relapse after IVIG administration

Slide101

Prognosis

3% mortality

Recovery- 1-6 months

80% have complete recovery in 12 months

Slide102

Polineuropathies

Diabetic neuropathy

Evaluation of peripheral neuropathies

Poliradiculoneuritis

Lumbar, sacrate and coccigeal plexus

Slide103

Distribution of roots from the Lumbar and Sacral Plexuses

Hip Flexion

L 1, 2, 3

Knee Extension

L 2, 3, 4

Foot Dorsiflexion

L 4,5

Foot Plantar Flexion

S1, 2

Knee Flexion

L5, S1, S2

Hip Extension

L5, S1, S2

Slide104

Dermatomes of the Leg

Slide105

Clinical Principles Reflexes

Detecting subtle weakness

Get up from squat

Quadriceps/Gluteus maximus

Stand on tip toes

Gastrocnemius/Soleus

Stand on heels

Tibialis Anterior

Knee Jerk - evaluates

Quadriceps muscle

Femoral Nerve

Primarily L4 nerve root (also L2, L3)

Ankle Jerk - evaluates

Gastrocnemius muscle

Tibial Nerve

Primarily the S1 nerve root (also S2)

Slide106

Lumbar Plexus

Formed by the anterior rami of L1-L4.

Supplies the anterolateral abdominal wall, external genitals, and part of the lower limbs.

Femoral nerves, obturator nerves.

Copyright 2009, John Wiley & Sons, Inc.

Slide107

Sacral Plexus

Formed by the anterior rami of L4-L5 and S1-S4.

Supplies the buttocks, perineum, and lower limbs.

Gives rise to the largest nerve in the body- the sciatic nerve.

Lies in pelvic cavity, anterior to sacrum and piriformis

Slide108

Branches

Superior gluteal

Pudendal

Posterior femoral cutaneous

Sciatic

Slide109

Gluteus maximus

Powerful hip extensor

Functions:

Climbing

Walking uphill

Regaining upright posture from squatting

NOT in normal walking

Hip (coxal) joint / GLUTEAL MUSCLE GROUP FUNCTIONS

Slide110

Coccygeal Plexus

Formed by the anterior rami of S4-S5 and the coccygeal nerves.

Supplies a small area of skin in the coccygeal region.

Copyright 2009, John Wiley & Sons, Inc.

Slide111

Obturator nerve

Enters thigh through obturator foramen;

Supplies medial group of muscles of thigh, obturator externus, and skin of medial side of thigh