Downloaded 30 times
Uploaded byQamar Zaman
Localization
This document discusses neurological examination and localization of lesions in the nervous system. It describes the steps in neurological diagnosis and provides information on localization of lesions at different levels of the neuraxis from the cortex to muscles. Key signs and symptoms are outlined for upper motor neuron and lower motor neuron lesions, as well as peripheral nerve disorders, neuromuscular junction disorders, and muscle disorders. Specific examination findings that help localize lesions in different parts of the brain, spinal cord, nerves, and neuromuscular junction are also summarized.
More Related Content
Localization
- 1. • Dr. QamarZaman FCPS(Neurology) Specialty Certified in Neurology Localization of the lesion in Neurological disorders
- 2. Steps in Neurologicaldiagnosis i. Recognition of impaired function. ii. Site of the nervous system has been affected. iii. The most likely etiology and list of D/D,s. iv. Ancillary procedures to determine the etiology.
- 3. Hypothesis • Initial hypothesis:all symptoms result from a focal lesion at one location • Bilateral symptoms and distributed over many body segments, consider a multifocal (eg multiple sclerosis) or diffuse (eg metabolic, toxic, ALS) disorder.
- 4. Divisions of theNeuraxis • Cortical Brain • Subcortical Brain • Brainstem • Cerebellum • Spinal Cord • Root • Peripheral Nerve • Neuromuscular Junction • Muscle
- 5. Scheme of localization •Determine whether its UMN or LMN issue. • Be aware that in acute cases spinal shock present may be as LMN signs. • Lesions of the premotor cortex, corona radiata, internal capsule, cerebral peduncle, basal pons, and lateral columns of the spinal cord.
- 6. Sequence of localization MuscleNMJ Peripheral nerve Brainstem spinal cord Basal ganglia Deep white matter Cortex
- 7. Facts about Localization •More precise for the lower levels of the nervous system. • It becomes less precise as we ascend.
- 8. Change over time •Findings from the lesions of the lower levels may change little/none over time. • The lesions of the higher levels may be very inconsistent/change over time.
- 9. Multifocal lesions • Theremay be more than one localizations eg : • MS, pt might have a lesion in the spinal cord and another lesion in the deep cerebral white matter.
- 10. Multifocal pathology • VitaminB12 deficiency cause combined myelopathy and neuropathy. • Should be confirmed or refuted by imaging, neurophysiology or laboratory testing.
- 11. Motor Signs andSymptoms and Their Localization • Plegia denotes complete paralysis while paresis denotes a lesser degree of weakness. • Common patterns of weakness include monoplegia (single limb weakness). • Hemiplegia (loss of motor function down one side of the body). • Paraplegia (bilateral loss of lower limb motor function).
- 12. • Quadriplegia ortetraplegia (loss of motor function in all four extremities). • Brachial diplegia (loss of motor function of both upper extremities), or facial diplegia (loss of motor function of both halves of the face).
- 13. • In peripheralnerve disorders the most common pattern of loss is that seen in peripheral neuropathies where the loss is mainly distal and affects the feet and hands in a glove and stocking distribution.
- 16. LMN • Weakness orparalysis of the involved muscles. • Flaccidity, hypotonia. • Diminished or absent muscle stretch reflexes (hyporeflexia or areflexia) and eventually atrophy.
- 17. • Muscle weakness,atrophy, fasciculations, and exaggerated muscle stretch reflexes suggest motor neuron disease. • Fasciculations, which are visible twitches of small groups of muscle fibers, may be present. • Pathologic reflexes cant be elicited.
- 18.
- 19.
- 20. Root value forreflexes
- 21. Anterior horn celldisease • In the spinal muscular atrophies, weakness and amyotrophy predominate in the proximal segments of the limbs, but distal, fascioscapulohumeral, scapulohumeral, and segmental forms are well known
- 22. Parsonage–Turner syndrome or neuralgicamyotrophy • Severe unilateral pain made worse with movement of the arm. • Minor sensory loss. • Weakness more proximal than distal. • Atrophy of muscles innervated by the upper trunk of the brachial plexus suggest a diagnosis of
- 23. Neurologic Examination whena Root is Lesioned Higher Cortical Function: normal Cranial Nerves: normal Cerebellar Function: normal Motor: assymetric weakness in a myotome Sensory: pain and dysesthesia confined to a dermatome Deep Tendon Reflexes: hypo- to a-reflexia if the root carries a reflex Pathologic Reflexes: none
- 24. • Inverted orparadoxical reflexes results from combined spinal cord and root (e.g., radiculomyelopathy). • As an example, with a C5–C6 lesion, when the biceps tendo is tapped, there is no biceps jerk, but the triceps contract (inverted biceps reflex).
- 25. Neurologic Examination withDiffuse PN Lesioning Higher Cortical Function: normal Cranial Nerves: normal Cerebellar Function: normal Motor: weakness is distal predominant Sensory: dysesthesias are distal predominant Deep Tendon Reflexes: loss of distal reflexes Pathologic Reflexes: mute responses to plantar stimulation
- 26. Neuropathies • Neuropathies aredivided into two main groups: • Mononeuropathies which involve single nerves. • Polyneuropathies which involve all nerves.
- 27. Neurologic Examination inDisorders of the NMJ Higher Cortical Function: normal Cranial Nerves: fatiguabile ptosis, dysconjugate gaze, slack jaw Cerebellar Function: normal Motor: fatiguable proximal weakness in both UE’s and LE’s Sensory: normal Deep Tendon Reflexes: normal Pathologic Reflexes: none
- 28. NEUROMUSCULAR JUNCTION • It resultsin a pattern of weakness which is characteristically fatigable on repeated testing. • The degree of weakness ranges from drooping of the eye lids and diplopia in mild cases to difficulty to talk, swallow, breathe, move eyes and limbs in severe cases.
- 29. Neurologic Examination inDisorders of Muscle Higher Cortical Function: normal Cranial Nerves: ptosis, dysconjugate gaze, dysphagia, dysphonia, (dysarthria) Cerebellar Function: normal Motor: proximal weakness in both UE’s and LE’s, atrophy and fasiculations, hypotonia Sensory: normal Deep Tendon Reflexes: preserved until late in the disease Pathologic Reflexes: none
- 30. MUSCLE • Muscle diseaseresults in weakness and sometimes muscle wasting. • Neurology examination is normal apart from the muscle weakness and reflexes are usually preserved until late in the disease when they may be lost.
- 31. • The clinicalcharacteristic of myopathic weakness is that the proximal muscles are more involved than the distal ones. • The main causes of muscle weakness are myopathy, polymyositis and muscular dystrophy.
- 33. UMN feaatures • Weaknessin upper extremity is most marked in extensors. • In lower extremity its most marked in hip flexors, knee flexors, foot dorsiflexors, and foot evertors.
- 34. • Spasticity predominatesin antigravity muscles (flexors UL and extensors LL). • Severe flexor or less-common extensor muscle spasms in response to a variety of nociceptive or nonnociceptive sensory stimuli, or may develop spontaneously.
- 35. • In braindisorders sensation is lost or more commonly altered on the side of the body opposite the site of lesion. The main causes are vascular and space occupying lesions.
- 36. • Patients withsevere spasticity may exhibit muscle deformities, contractures, and associated reactions including synkinesias.
- 40. • If thereis facial weakness of the upper motor neuron on the same side of the hemiplegia, the lesion is generally localizable above the upper pons. • likely sites are the MC, corona radiata, or internal capsule.
- 41. Weakness • The faceand arm weak > the leg, the lesion is often corticosubcortical and laterally placed on the contralateral hemisphere. • If the leg is more severely >arm and face weakness the lesion most likely involves the contralateral paracentral region. • In cases of internal capsule lesions, the hemiplegia is often proportionate, with equal involvement of the face and upper and lower limbs.
- 42. • Cranial nerveson one and weakness on contralateral side point to lesion below cerebral peduncle • However, a lesion on the cerebral peduncles and upper pons can also cause a hemiplegia or hemiparesis with an associated upper motor neuron type of facial paresis.
- 43. Hemiparesis • Determine weaknessand cranial nerves involvement are on same side or opposite. • When a patient presents with hemiplegia or hemiparesis, it is important to determine whether the lower half of the face is involved with relative sparing of upper facial function.
- 47. • Spinal cordlesions are often associated with marked flexor spasms, may also be accompanied by bladder and, occasionally, fecal incontinence. • Other features include muscle weakness, muscle slowness, impaired dexterity, and fatigability.
- 48. • In corddisorders the loss involves the limbs (usually the legs) and the trunk below the level of the lesion. • The extent and pattern of loss depends on the underlying lesion, e.g. complete or partial cord involvement resulting in paraplegia. • The main causes are trauma and infection.
- 49. • A lesionaffecting one half of the spinal cord results in a hemi section or a Brown-Sequard syndrome. • This has three main and diagnostic neurological features all occurring below the level of the lesion. These are a loss of power (UMNL) and a loss of joint position sense and vibration occurring on the same side as the lesion and a loss of pain and temperature on the opposite side the lesion.
- 50. • A lesioncausing a complete transverse section of the cord results in a total loss of power and feeling below the level of the lesion and loss of bowel and bladder control
- 54. Thoracic spinal cord Spasticparaparesis or paraplegia with bilateral Babinski’s sign. sensory level in thoracic area; urinary retention; loss of position sense in feet (unless anterior spinal artery syndrome, in which posterior column function spared).
- 55. Conus medullaris FUNCTION: bladderand bowel function. COMMON LESIONS: usually tumours in region of L1. LESIONS RESULT IN: Saddle anaesthesia, bladder and bowel dysfunction, pain in legs may occur late in course.
- 56. Cauda equina FUNCTIONS: Sensoryand motor function in legs, bladder and bowel function. COMMON LESIONS: Usually herniated lumbar disks or meningeal cancer. LESIONS RESULT IN: Scattered pain and weakness in legs, loss of knee and/or ankle reflexes, bladder and bowel dysfunction.
- 57. • The lesionsof the conus medullaris result in early sphincter compromise, late pain, and symmetrical sensory manifestations, • cauda equina lesions have late sphincter manifestations, early pain, and asymmetricalsensory findings, this distinction is often exceedingly difficult to establish and is of little practical value.
- 61. Generalized weakness • Generalizeddistal weakness is likely to be due to a peripheral neuropathy, although proximal weakness occurs in some cases and can imitate myopathy. • Generalized proximal weakness is likely to be due to a myopathy or neuromuscular junction disorder
- 62. • Fluctuating weakness,extraocular muscles and proximal limb muscles, worse with exercise and better with rest, is the hallmark of myasthenia gravis.
- 63. • Symmetric upperand lower girdle muscle involvement associated with muscle pain and dysphagia is often seen in patients with idiopathic inflammatory myopathies.
- 64. • Asymmetric distal(e.g., foot extensors and finger flexors) and proximal (e.g., quadriceps) weakness may be a clue to the diagnosis of inclusion body myositis. • Delayed relaxation of skeletal muscle following voluntary contraction is present in myotonic disorders.
- 65. • Episodic attacksof flaccid limb muscle weakness, with sparing of ocular and respiratory muscles, are characteristic of periodic paralysis. • Pseudohypertrophy of the calves is seen in most boys with Duchenne’s muscular dystrophy.
- 66. • The Gowers’maneuver, resulting from weakness in the proximal hip muscles, may be observed, with affected patients using their hands to rise from the ground. • Other early features include hyperlordosis of the lumbar spine and a waddling wide-based gait and toe walking.
- 67. Psychogenic hemiplegia • Inpsychogenic hemiplegia, the lower half of the face ipsilateral to the hemiplegia is not involved. • The protruded tongue, if it deviates at all, deviates toward the normal side . • The abdominal, plantar, and muscle stretch reflexes are always normal.
- 68. Psychogenic weakness • Thehand is not preferentially affected as in organic hemiplegia. • The side-gait (patient is asked to move sideways along a straight line) is as a rule equally impaired in both directions alike.
- 69. Final steps inlocalization • The final localization hypothesis – or top two localizations – is made. • Localization based on the clinical findings is confirmed by the neuroimaging or neurophysiology test results.