Neurology (eBook)

Heinrich Mattle, Ethan Taub, Marco Mumenthaler (Herausgeber)

eBook Download: EPUB

2003 | 4. Auflage
1008 Seiten
Georg Thieme Verlag KG
978-3-13-258134-0 (ISBN)

Infos

<p>Pocket-sized and affordable, this classic Thieme Flexibook provides a thorough and comprehensive review of clinical neurology. The fully revised fourth edition puts new emphasis on clinical relevance, and contains updated information on stroke, epilepsy, eye movements, headache, and more!</p><p>Key features:</p><ul><li> Nearly 1,000 pages of up-to-date clinical information <li> More than 50% of the book has been totally revised and updated for this edition <li> Easy-to-use index provides quick access to content <li> Written by two experienced clinical neurologists and teachers</li></ul><p>One of the best basic works to address the entire field of neurology, this practical book has become a major text and reference for neurology students and residents the world over. The book also appeals to general practitioners, neurology specialists, and even neurosurgeons needing a quick reference on an unfamiliar neurological problem.</p>

Mark Mumenthaler, Heinrich Mattle

Textauszug

1 Clinical Syndromes in Neurology

Because of the anatomical construction of the nervous system and the manner in which functions are assigned to its components, lesions in specific areas of the central or peripheral nervous system are regularly associated with characteristic symptoms and signs. An acquaintance with these recurring patterns allows one to trace individual findings or constellations of findings back to the responsible dysfunctional component of the nervous system (Table 1.1).

Table 1.1 Components of the nervous system

Central

Peripheral

Brain (not including cranial nerve nuclei)

Cranial nerve nuclei

Spinal cord (not including anterior horn ganglion cells)

Anterior horn ganglion cells Nerve roots Brachial and lumbar plexuses Peripheral nerves Motor end plates Muscles

The following discussion will concern the most important typical constellations of findings (syndromes):

central paresis,

peripheral paresis,

monoparesis,

hemiparesis,

paraparesis,

quadriparesis,

anterior horn lesion,

radicular lesion,

polyradiculopathy,

polyneuropathy,

plexus lesion,

lesion of a single peripheral nerve,

dysfunction of the neuromuscular junction (motor end plate),

myopathy.

Differentiation of Central and Peripheral Paresis

Central and peripheral forms of paresis may be differentiated from each other by the criteria listed in Table 1.2.

Table 1.2 Characteristics of central and peripheral paresis

Feature

Central paresis

Peripheral paresis

Proprioceptive muscle reflexes

Increased

Decreased

Exteroceptive muscle reflexes

Decreased

Decreased

Babinski sign

Present

Absent

Muscle atrophy

Absent (or mild atrophy of disuse)

Present

Muscle tone

Increased (i.e., spasticity; not yet present in acute phase)

Decreased

Bodily Distribution of Paresis

The distribution of paresis in the body enables a number of inferences to be made about the nature and anatomical localization of the responsible lesion.

Monoparesis

Monoparesis is defined as isolated weakness of an entire limb or of a major part of it. Possible causes are listed in Table 1.3.

Table 1.3 Sites of lesions causing monoparesis, and corresponding clinical features

Site of lesion

Clinical features

Central nervous system

Spastic paresis (increased muscle tone, increased reflexes) No muscle atrophy Possibly a purely motor deficit (e.g., contralateral leg paresis due to ischemia in the territory of the anterior cerebral artery)

Anterior horn of spinal cord(chronic lesion)

Paresis of individual muscles with accompanying atrophy and decreased tone No sensory deficit Possibly accompanied by fasciculations Decreased proprioceptive muscle reflexes (but may be increased in amyotrophic lateral sclerosis)

Brachial or lumbar plexus

Mixed sensory and motor deficit Decreased muscle tone Muscle atrophy, decreased proprioceptive muscle reflexes Sensory deficit for all modalities

Multiple peripheral nerves

Same as in plexus lesions in a single limb

Muscle

Hardly ever a pure monoparesis; if so, then flaccid Purely motor deficit, sometimes with muscle atrophy

Hemiparesis

Hemiparesis may be due to any of the causes listed in Table 1.4.

Para- and Quadriparesis

Paraparesis is weakness affecting both lower limbs, and quadriparesis is weakness affecting all four limbs (but sparing the head). These may be due to any of the causes listed in Table 1.5.

Table 1.4 Sites of lesions causing hemiparesis, and corresponding clinical features

Site of lesion

Clinical features

Cerebrum

Spastic hemiparesis, possibly also involving facial muscles, characterized by: Increased muscle tone Increased reflexes Pyramidal tract signs No atrophy Usually associated with a sensory deficit

Brain stem

Spastic hemiparesis, as above Face involved or not, depending on level of lesion Cranial nerve deficits contralateral to hemiparesis

Upper cervical spinal cord

Spastic hemiparesis, as above Face spared Possible ipsilateral loss of position and vibration sense and contralateral loss of pain and temperature sense below the level of the lesion (Brown-Sequard syndrome)

Table 1.5 Sites of lesions causing para- or quadriparesis,and corresponding clinical features

Site of lesion

Clinical features

Cerebrum (bilateral lesion)

Clinical picture of “bilateral hemiparesis,” or paraparesis due to a bilateral parasagittal cortical lesion

Corticobulbar pathways in the brain stem (bilateral lesion) (e.g., lacunar state, p. 178)

Bilateral spasticity with only mild weakness Spastic, small-stepped gait hyperreflexia, pyramidal tract signs No sensory deficit Usually accompanied by pseudobulbar signs (dysarthria, hyperreflexia of the facial musculature)

Corticospinal pathways in the spinal cord (bilateral lesion)

Para- or quadriparesis Face spared Hyperreflexia, pyramidal tract signs No sensory deficit Only mild weakness

Lesions Affecting the Anterior Horn Ganglion Cells

Lesions selectively affecting the efferent neurons (ganglion cells) of the anterior horn of the spinal cord (p. 425 ff.) produce the characteristic clinical findings listed in Table 1.6.

Table 1.6 Clinical features of an isolated lesion of the anterior horn ganglion cells

Muscle atrophy

Weakness

Fasciculations (in chronic phase)

Intact sensation

Decreased or absent reflexes

But: hyperreflexia and pyramidal tract signs in amyotrophic lateral sclerosis, which involves not only the anterior horns but also the corticospinal pathways (thus the term “lateral” sclerosis, as these pathways are lateral in the spinal cord)

Lesions Affecting a Spinal Nerve Root

Lesions affecting a spinal nerve root (p. 717 ff.) always produce both motor and sensory deficits. Individual spinal nerve roots always supply more than one muscle, and no muscle is supplied exclusively by a single root. Thus, the motor deficit produced by a monoradicular lesion has the following characteristics:

There is always more than one affected muscle.

No affected muscle is ever totally paralyzed.

Nevertheless, certain muscles are predominantly supplied by a single root and are, therefore, weakened to a particularly severe degree by a corresponding monoradicular lesion. Proprioceptive muscle reflexes partially subserved by the affected root may be decreased or even absent (cf. Table 1.4). The sensory deficit lies within the corresponding sensory dermatome (cf. Table 1.1) and thus usually has a band-like cutaneous distribution. Pain, if present, is referred into the dermatome of the affected root. Although the deficit is mixed (both motor and sensory), the clinical picture may be dominated by either the motor deficit or the sensory deficit in individual cases. Atrophy of the affected muscles is evident about 3 weeks after the onset of weakness.

Fig. 1.1a-g Cutaneous sensation.

Fields of sensory innervation of peripheral nerves and spinal nerve roots, depicted on the left and right sides of the body, respectively.

1 Trigeminal n.

2 Great auricular n.

3 Transverse cutaneous n.

4 Supraclavicular nn.

5 Anterior cutaneous branches of the intercostal nn.

6 Superior lateral cutaneous...

Produkt-Details

• Erscheint lt. Verlag: 10.12.2003
• Verlagsort: Stuttgart
• Sprache: englisch
• Themenwelt: Medizin / Pharmazie ► Medizinische Fachgebiete ► Neurologie
• Schlagworte: Neurology
• ISBN-10: 3-13-258134-8 / 3132581348
• ISBN-13: 978-3-13-258134-0 / 9783132581340