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Cerebrovascular Ultrasonography, Diagnostic Imaging, and Biopsy Procedures

Aspect To Be Tested

Questions/Tests

!

Attention (p. 116)

! Awake, somnolent, stuporous, comatose? Arousability, attention

 

 

span, perception

!

Orientation

! Personal data (name, age, date/place of birth), orientation (“where

 

 

are we?”, place of residence); time (day of the week, date, month,

 

 

year); situation (reason for consultation, nature of symptoms)

!

Memory, recall

! The patient should be able to name the months of the year back-

 

 

ward, spell a word backward, repeat random series of numbers be-

 

 

tween 1 and 9. Can the patient recall 3 objects mentioned 3

 

 

minutes ago, recall figures, name famous people? Tests of general

 

 

knowledge

!

Serial subtraction

! Serial subtraction of 3s (or 7s), starting from 100

!

Frontal lobe function

! Perseveration1; hand sequence test2; proverb interpretation

!

Language (pp. 124, 128)

! Following commands, naming, repetition, writing, reading aloud,

 

 

simple arithmetic

!

Praxis

! See p. 128

!Spatial orientation, visual percep- ! See p. 132. Naming of colors and objects tion

(After Schnider, 1997) 1 Drawing of simple figures (Luria’s loops). 2 Command sequence: “Make a fist—open the hand to the side—open the hand flat.”

" Cerebrovascular Ultrasonography

Ultrasound can be used to assess the extracranial and intracranial arteries. The transmitter emits ultrasonic waves in two modes, continuous wave (CW; cross-sectional data, but no depth information) and pulse wave (PW; flow information at different levels). The reflected waves are recorded (echo impulse signal) and analyzed (frequency spectrum analysis, color coding). The flow velocity of blood particles can be determined according to the Doppler principle. As the flow velocity is correlated with the diameter of a blood vessel, its measurement reveals whether a vessel is stenotic. In direct vessel recordings, CW Doppler can be used to determine the direction of flow and the presence or absence of stenosis or occlusion. In duplex sonography, the PW Doppler and ultrasound images (echo impulse) are combined for simultaneous demonstration of blood flow (color-coded flow image) and tissue structures (tissue image). This permits visualization and

quantitation of stenosis, dissection, extracranial vasculitis, and vascular anomalies. Transcranial Doppler (TCD) and duplex sonography are used to study the intracranial arteries, e. g., for stenosis, occlusion, collateral flow, vasospasm (after subarachnoid hemorrhage), shunting (arteriovenous malformation or fistula), and hemodynamic reserve.

" Neuroimaging

The neuroradiologist can demonstrate structural changes associated with neurological disease with a number of different imaging techniques. When a patient is sent for a neuroimaging study, the reason for ordering the study and the question(s) to be answered by it must be clearly stated. Interventional procedures in the neuroradiology suite are mainly performed to treat vascular lesions (embolization of an arteriovenous malformation, fistula, or aneurysm; thrombolysis; angioplasty; devascularization of neoplasms; stent implantation).

Diagnostic Evaluation

353

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Diagnostic Evaluation

Cerebrovascular Ultrasonography, Diagnostic Imaging, and Biopsy Procedures

Imaging Study

Indication/Objective1

Conventional radiography2

Skull, spine

Computed tomography (CT)

Head, spine, spinal canal, CT-guided diagnostic interventions, 3-D reconstruction

Magnetic resonance imaging (MRI)4

!Head, spine, spinal canal

!Skeletal muscle

Angiography3,5

Cerebral, spinal; preinterventional or preoperative study6

Myelography3,7

Diagnostic nuclear medicine

!Skeletal scintigraphy (“bone scan”)

!CSF scintigraphy

!Emission tomography8

Metallic foreign bodies, air-filled cavities, fractures, skull defects, bony anomalies, osteolysis, spinal degenerative disease

Assessment of skeleton (anomalies, fractures, osteolysis, degenerative changes, spinal canal stenosis), metastases, trauma, intracranial hemorrhage, cerebral ischemia, hydrocephalus, calcification, intervertebral disk disease, contrast studies3 (brain, spinal canal, CT angiography)

!Tumors (brain, spine, spinal cord), infection (encephalitis, myelitis, abscess, AIDS, multiple sclerosis), structural anomalies of the brain (epilepsy), leukodystrophy, MR angiography (aneurysm, vascular malformation), ischemia of the brain or spinal cord, spinal trauma, hydrocephalus, myelopathy, intervertebral disk disease

!Muscular atrophy, myositis

High-grade arterial stenosis, aneurysm, arteriovenous malformation/ fistula, sinus thrombosis, vasculitis

Largely replaced by CT and, especially, MRI. Used to clarify special diagnostic questions in spinal lesions

!Tumor metastasis, spondylodiscitis

!Intradural catheter function test, CSF leak

!Cerebral perfusion, cerebral metabolic disorders, degenerative diseases, diagnosis of epilepsy

1 Examples. 2 Plain radiographs, X-ray tomography. 3 Risks: allergy ( intolerance), latent hyperthyroidism ( thyrotoxicosis), thyroid carcinoma ( radioiodine therapy cannot be performed for a long time afterward), renal failure, left heart failure ( pulmonary edema), plasmacytoma ( renal failure). 4 Gadolinium contrast agent can be used to show blood–brain barrier lesions (e. g., acute multiple sclerosis plaques). T1-weighted scans: CSF/ edema dark (hypointense), diploe/fat light (hyperintense), white matter light; gray matter dark. T2-weighted scans: CSF/edema light, scalp dark, diploe/fat light, muscle dark, white matter dark; gray matter light. Contraindications: Cardiac pacemaker, mobile ferromagnetic material. 5 Contraindicated in patients with coagulopathy. 6 Endovascular or surgical therapy. 7 Rare complications: generalized epileptic seizures, meningitis, post–lumbar puncture headache; acute transverse cord syndrome possible in patients with spinal tumors. Coagulopathy is a contraindication. 8 SPECT = single-photon emission computed tomography, PET = positron emission tomography.

" Tissue Biopsy

vessels (e. g., the temporal artery in suspected

temporal arteritis). These biopsies can usually

 

In certain cases, the provision of a definitive di-

be carried out under local anesthesia. Spinal

agnosis requires biopsy of nerve (usually the

tumors can be biopsied under CT or MRI

sural nerve, p. 391), muscle (a moderately af-

guidance, and brain tumors and abscesses can

fected muscle in myopathy, p. 399), or blood

be biopsied with stereotactic technique.

354

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5 Appendix

!Supplementary tables

!Detailed information

!Outlines

!Working aids

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Appendix

Appendix

Table 1 Cranial nerves (p. 28)

Pathway

Cranial Nerve (CN)/Nucleus

Functions

 

 

 

 

Somatosensory

II

Retina

Vision

(afferent)

III

Proprioceptors of extraocular mm.1

Proprioception2

 

IV

Proprioceptors of extraocular mm.

Proprioception

 

V

Semilunar ganglion, proprioceptors

Sensation in face, nose, nasal cavity, oral

 

 

of masticatory, tensor veli palatini,

cavity; proprioception, dura mater (pp. 6,

 

 

and tensor tympani muscles

94)

 

VI

Proprioceptors of extraocular mm.

Proprioception

 

VII

Geniculate ganglion

External ear, parts of auditory canal, outer

 

 

 

surface of eardrum (sensation)

 

VIII

Vestibular ganglion; spiral ganglion

Balance/equilibrium; hearing

 

IX

Superior ganglion

Middle ear, auditory tube (sensation)

 

X

Superior ganglion

External auditory canal/dura mater of

 

 

 

posterior fossa (p. 5)

Visceral (afferent)

I

Olfactory cells of nasal mucosa

Smell

 

VII

Geniculate ganglion

Taste on anterior 2/3 of tongue (chorda

 

 

 

tympani), taste on inferior surface of soft

 

 

 

palate (greater petrosal n.)

 

IX

Inferior and superior ganglia

Taste/sensation on posterior 1/3 of

 

 

 

tongue, pharyngeal mucosa, tonsils, audi-

 

 

 

tory tube (sensation)

 

X

Inferior ganglion

Abdominal cavity (sensation), epiglottis

 

 

 

(taste)

Motor (efferent)

III

Oculomotor nucleus3

Extraocular mm. (except those supplied

 

 

 

by CN IV, VI), raise eyelid (levator palpe-

 

 

 

brae superioris m.)

 

IV

Trochlear nucleus

Oblique eye movements (superior oblique

 

 

 

m.)

 

V

Motor nucleus of trigeminal n.

Mastication,4 tensing of palate5 and tym-

 

 

 

panic membrane6

 

VI

Abducens nucleus

Lateral eye movements (lateral rectus m.)

 

VII

Facial nucleus

Facial muscles, platysma, stylohyoid and

 

 

 

digastric muscles

 

IX

Nucleus ambiguus

Pharyngeal mm., stylopharyngeus m.

 

X

Nucleus ambiguus

Swallowing (pharyngeal mm.), speech

 

 

 

(superior laryngeal nerve)

 

XI

Nucleus ambiguus, motor cells of

Muscles of pharynx and larynx, sternoclei-

 

 

anterior horn of cervical spinal cord

domastoid m.7 trapezius m.8

 

XII

Hypoglossal nucleus

Muscles of tongue

Visceral (efferent)

III

Parasympathetic, Edinger–Westphal

Pupillary constriction (sphincter pupillae

 

 

nucleus

m.), accommodation (ciliary m.)

 

VII

Parasympathetic, superior salivatory

Secretion of mucus, tears, and saliva (sub-

 

 

nucleus

lingual and submandibular glands)

 

IX

Parasympathetic, inferior salivatory

Secretion of saliva (parotid gland)

 

 

nucleus

 

 

X

Parasympathetic, dorsal nucleus of

Lungs, heart, intestine to left colonic

 

 

vagus nerve

flexure (motor); glandular secretion (res-

 

 

 

piratory tract, intestine)

 

 

 

 

1 Eye muscles. 2 See p. 104. 3 Nucleus. 4 Masseter, temporalis, lateral pterygoid, and medial pterygoid muscles. 5 Tensor veli palatini m. 6 Tensor tympani m. 7 Shoulder elevation, scapular fixation, accompanying movements of cervical spine. 8 Neck flexion and extension, head rotation.

356

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Appendix

Table 2 Segment-indicating muscles (p. 32)

Segment

Segment-indicating Muscle(s)

 

 

C4

Diaphragm

C5

Rhomboids, supraspinatus, infraspinatus, deltoid

C6

Biceps brachii, brachioradialis

C7

Triceps brachii, extensor carpi radialis, pectoralis major, flexor carpi radialis, pronator

 

teres

C8

Abductor pollicis brevis, abductor digiti quinti, flexor carpi ulnaris, flexor pollicis brevis

L3

Quadriceps femoris, iliopsoas; adductor longus, brevis et magnus

L4

Quadriceps femoris (vastus medialis m.)

L5

Extensor hallucis longus, tibialis anterior, tibialis posterior, gluteus medius

S1

Gastrocnemius, gluteus maximus

 

 

Tables 3 Types of tremor (p. 62)

Type

Features

 

 

Physiological tremor (PT)

Normal. Discrete, usually asymptomatic tremor of unclear significance.

 

Isometric tremor may occur, e. g., when holding a heavy object.

Exaggerated PT, toxic or drug-

Amplitude !PT, frequency = PT. Absent at rest. Mainly PosT.1 Stress

induced tremor

(anxiety, fatigue, excitement, cold). Metabolic disturbances (hyperthyroidism,

 

hypoglycemia, pheochromocytoma). Drugs/toxins (alcohol or drug with-

 

drawal; mercury, manganese, lithium, valproic acid, cyclosporine A, amio-

 

darone, flunarizine, cinnarizine, tricyclic antidepressants, neuroleptics tar-

 

dive tremor)

Essential tremor (ET)

Classical ET: PosT !KT 2. Approx. 60% autosomal dominant, rest sporadic.

 

Hands !head !voice !trunk. Often improved by alcohol.

 

Orthostatic tremor: Occurs only when standing unsteadiness, hard to

 

stand still.

 

Task-specific tremor

Parkinsonian tremor

RT 3 See p. 206. Postural and kinetic tremor may also be present.

Cerebellar tremor

IT4 reflecting cerebellar dysfunction. Postural tremor and head/trunk tremor

 

may be seen when the patient is standing (alcohol intoxication).

Holmes tremor (rubral, mid-

RT + PosT + IT, mainly proximal, disabling. Associated with lesions of nigro-

brain tremor, myorhythmia)

striatal and cerebello-thalamic pathways (multiple sclerosis, infarct)

(Poly-)neuropathic tremor

RT, PosT, or IT, predominantly either proximal or distal. 3–10 Hz5

Palatal tremor

Symptomatic (medullary lesion due to encephalitis, multiple sclerosis, brain

 

stem infarct) or essential; clicking noise in ear

Psychogenic tremor

Migrates from one part of the body to another. Accompanied by muscle

 

contraction (co-contraction)

 

 

1 PosT = postural tremor. 2 KT = kinetic tremor. 3 RT = resting tremor. 4 IT = intention tremor. 5 Occurs in hereditary sensorimotor neuropathy type I, chronic demyelinating polyradiculitis, paraproteinemic neuropathy, diabetic neuropathy, and uremic neuropathy.

Appendix

357

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Appendix

358

Appendix

Table 4 Midbrain syndromes (p. 71)

Anterior Midbrain Lesions (Peduncle, Weber Syndrome)

Cause. Infarct. Less commonly caused by hemorrhage, tumor (germinoma, teratoma, pineocytoma, pineoblastoma, astrocytoma, tentorial edge meningioma, lymphoma), or multiple sclerosis.

Structure Affected

Symptoms and Signs

 

 

Intramesencephalic fibers of

Ipsilateral oculomotor paralysis + parasympathetic dysfunction (pupil dilated

oculomotor n.

and unreactive to light)

Pyramidal tract

Contralateral central paralysis + face ( supranuclear facial palsy) + spastic-

 

ity. Dysarthria (supranuclear hypoglossal palsy)

Substantia nigra

Rigidity (rare)

 

 

Medial Midbrain Lesions (Tegmentum, Benedikt Syndrome)

Cause. Same as in anterior lesions.

Structure Affected

Symptoms and Signs

 

 

Intramesencephalic fibers of

Ipsilateral oculomotor paralysis + parasympathetic dysfunction (see above )

oculomotor n.

 

Medial lemniscus

Contralateral impairment of touch, position, and vibration sense

Red nucleus

Contralateral tremor (myorhythmia red nucleus syndrome, Holmes

 

tremor)

Substantia nigra

Rigidity (variable)

Superior cerebellar peduncle

Contralateral ataxia ( Claude syndrome)

 

 

Dorsal Midbrain Lesions (Tectum, Parinaud Syndrome)

Cause. Tumor of third ventricle, infarct, arteriovenous malformation, multiple sclerosis, large aneurysm of posterior fossa, trauma, shunt malfunction, metabolic diseases (Wilson disease, Niemann–Pick disease), infectious diseases (Whipple disease, AIDS)

Structure Affected

Symptoms and Signs

 

 

Oculomotor nuclei

Pathological lid retraction (Collier’s sign) due to overactivity of levator

 

palpebrae superioris m. Over the course of the disease, accommodation is

 

impaired; the pupils become moderately dilated and unreactive to light, but

 

they do constrict on convergence (light-near dissociation)

Medial longitudinal fasciculus

Supranuclear palsy of upward conjugate gaze (vertical gaze palsy the

 

eyes move upward on passive vertical deflection of the head, but not volun-

 

tarily). Convergence nystagmus with retraction of the eyeball on upward

 

gaze (retraction-convergence nystagmus)

Trochlear nucleus

Trochlear nerve palsy

Aqueduct (compressed)

Hydrocephalus (headache, papilledema)

 

 

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Appendix

Table 4 Midbrain syndromes (continued)

Top of the Basilar Artery Syndrome

Cause. Large aneurysm of the basilar tip, thromboembolism in the upper basilar territory, vasculitis, complication of angiography. (Central paralysis is not found.)

Site of Lesion

Symptoms and Signs

 

 

Midbrain

Unilateral or bilateral vertical gaze palsy; impaired convergence; retraction

 

nystagmus. Sudden oscillations (sensation of movement of surroundings

 

when walking or when moving head). Collier’s sign. Strabismus with di-

 

plopia. Pupils may be constricted and responsive or dilated and unrespon-

 

sive to light.

Thalamus, parts of temporal

Visual field defects (homonymous hemianopsia, cortical blindness). Variable

and occipital lobes

features: Somnolence, peduncular hallucinations (dreamlike scenic halluci-

 

nations), memory impairment, disorientation, psychomotor hyperactivity

 

 

Table 5 Pontine syndromes (p. 72)

Anterior Pontine Lesions (Ventral Pons)

Cause. Basilar artery thrombosis, hemorrhage, central pontine myelinolysis, brain stem encephalitis, tumors, trauma. Arterial hypertension (lacunar infarct).

! Mid Ventral Pons

Structures Affected

Symptoms and Signs

 

 

Pyramidal tract

Contralateral central paralysis sparing the face

Intrapontine fibers of trigemi-

Ipsilateral facial hypesthesia, peripheral-type weakness of muscles of mas-

nal nerve

tication

Middle cerebellar peduncle

Ipsilateral ataxia

 

 

! Lacunar Syndromes1

Structures Affected

Symptoms and Signs

 

 

Pyramidal tract

Contralateral central paralysis, sometimes more pronounced in legs, with or

 

without facial involvement

Middle cerebellar peduncle

Ipsilateral ataxia, which may be accompanied by dysarthria and dysphagia,

 

depending on the site of the lesion (dysarthria—clumsy hand syndrome)

 

 

1Similar syndromes can also occur in patients with supratentorial lacunas (internal capsule, thalamocortical pathways).

! Locked-in Syndrome (p. 120)

Structures Affected

Ventral pons (corticobulbar and corticospinal tracts) bilaterally, abducens nucleus, pontine paramedian reticular formation, fibers of trigeminal nerve

Symptoms and Signs

Quadriplegia, aphonia, inability to swallow, horizontal gaze palsy (including absence of caloric response), absence of corneal reflex (risk of corneal ulceration)

Eyelid and vertical eye movements (supranuclear oculomotor tracts), sensation, wakefulness (reticular ascending system), and spontaneous breathing remain intact.

Appendix

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Appendix

360

Appendix

Table 5 Pontine syndromes (continued)

Dorsal Pontine Lesions (Pontine Tegmentum)

Cause. Same as in lesions of ventral pons.

! Oral (Superior) Pontine Tegmentum (Raymond–Céstan Syndrome)

Structures Affected

Symptoms and Signs

 

 

Trigeminal nucleus/fibers

Ipsilateral facial hypesthesia, peripheral paralysis of muscles of mastication

Superior cerebellar peduncle

Ipsilateral ataxia, intention tremor

Medial lemniscus

Contralateral impairment of touch, position, and vibration sense

Spinothalamic tract

Contralateral loss of pain and temperature sensation

Paramedian pontine reticular

Ipsilateral loss of conjugate movement (loss of optokinetic and vestibular

formation (PPRF, “pontine

nystagmus PPRF lesion with intact vestibulo-ocular reflex (VOR, p. 84))

gaze center”)

 

Pyramidal tract

Contralateral central paralysis sparing the face

 

 

! Caudal Pontine Tegmentum

Structures Affected

Symptoms and Signs

 

 

Pyramidal tract

Contralateral central paralysis sparing the face

Nucleus/fibers of the facial n.

Ipsilateral (nuclear = peripheral) facial palsy ( Millard–Gubler syndrome)

Fibers of abducens nerve

Ipsilateral abducens paralysis ( Foville syndrome, eyes drift “away from

 

the lesion”; loss of VOR)

Central sympathetic pathway

Ipsilateral Horner syndrome

PPRF

Loss of ipsilateral conjugate movement

Medial and lateral lemniscus

Contralateral impairment of touch, position, and vibration sense

Lateral spinothalamic tract

Contralateral impairment of pain and temperature sensation

 

 

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Appendix

Table 6 Medullary syndromes (p. 73)

Medial Medullary Lesions

Cause. Occlusion of the anterior spinal artery or vertebral artery.

Structures Affected

Symptoms and Signs

 

 

Hypoglossal n. nucleus/fibers

Ipsilateral peripheral (nuclear) hypoglossal paralysis

Pyramidal tract

Contralateral central paralysis sparing the face (flaccid, in isolated pyramidal

 

tract lesions)

Medial lemniscus

Contralateral impairment of touch, position, and vibration sense (pain and

 

temperature sensation intact)

Medial longitudinal fasciculus

Upbeat nystagmus

 

 

Lateral Medullary Lesions (Dorsolateral Medullary Syndrome, Wallenberg Syndrome)

Cause. Occlusion of posterior inferior cerebellar artery (PICA) or vertebral artery. Less common causes: tumor, metastases, hemorrhage due to vascular malformations, multiple sclerosis, vertebral artery dissection (after chiropractic maneuvers), trauma, gunshot wounds, cocaine intoxication.

Site of Lesion

Symptoms and Signs

 

 

Spinal nucleus of trigeminal

Ipsilateral analgesia/thermanesthesia of the face and absence of corneal re-

nerve

flex with or without facial pain

Cochlear nucleus

Ipsilateral hearing loss

Nucleus ambiguus

Ipsilateral paralysis of the pharynx and larynx (hoarseness, paralysis of the

 

soft palate), dysarthria, and dysphagia. Tongue movement remains intact

Solitary nucleus

Ageusia (impaired sense of taste)

Dorsal nucleus of vagus n.

Tachycardia and dyspnea

Inferior vestibular nucleus

Nystagmus away from the side of the lesion, tendency to fall toward the

 

side of the lesion, nausea and vomiting

Central tegmental tract

Ipsilateral myorhythmia of the soft palate and pharynx

Central sympathetic pathway

Ipsilateral Horner syndrome

Reticular formation

Singultus

Inferior cerebellar peduncle

Ipsilateral ataxia and intention tremor

Anterior spinocerebellar tract

Ipsilateral hypotonia

Lateral spinothalamic tract

Contralateral loss of pain and temperature sensation with sparing of touch,

 

position, and vibration sense (sensory dissociation)

 

 

Involvement of the lower pons produces diplopia. Occipital pain in Wallenberg syndrome is most commonly due to vertebral artery dissection.

Appendix

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Appendix

362

Appendix

Table 7 Syndromes affecting the facial muscles (p. 98)

Syndrome

 

Etiology

 

 

 

Hypomimia or amimia

 

Basal ganglia dysfunction (p. 206), depression

Blepharospasm, Meige syndrome, lid-opening

Basal ganglia dysfunction

apraxia, oromandibular dystonia, tics (p. 64ff.)

 

Melkersson–Rosenthal syndrome (recurrent swelling

Unknown

of face/lips, peripheral facial palsy, and fissured

 

tongue)

 

 

Heerfordt syndrome (fever, uveitis, parotitis, periph-

Occasional manifestation of sarcoidosis, lymphoma.

eral facial palsy)

 

Cryptogenic

Bilateral peripheral facial paralysis

 

Neuroborreliosis, Guillain–Barré syndrome, Fisher

 

 

syndrome, botulism

Möbius syndrome

 

Congenital bilateral facial palsy and cranial nerve in-

 

 

volvement (bilateral: VI; unilateral: XII, IV, VIII, IX)

Synkinesis (involuntary co-movement of facial

Faulty regeneration of CN VII after facial palsy. Nerve

muscles, e. g., narrowing of palpebral fissure when

root compression and segmental demyelination in

the lips are pursed); hemifacial spasm

 

hemifacial spasm

Pseudobulbar palsy

 

Multiple bilateral supratentorial or pontine vascular

 

 

lesions

Myopathic facies

 

Myopathic disorders (myotonic dystrophy, my-

 

 

asthenia, facial-scapular-humeral muscular dystrophy)

Gustatory sweating (Frey syndrome) or lacrimation

Faulty regeneration of the auriculotemporal/facial

(“crocodile tears”)

 

nerve

Progressive facial hemiatrophy

 

Unknown

Table 8 Neurological Causes of Dysphagia (p. 102)

 

 

 

 

Symptoms and Signs

Site of Lesion

Cause

Oral phase impaired and swallow-

Supratentorial

Cerebral infarct, tumor or hemorrhage

ing reflex delayed (slightly) be-

Unilateral

 

cause of paralysis

 

 

Delayed swallowing reflex, aspira-

Supratentorial

Vascular lesions (single or multiple infarcts, hemor-

tion (especially of fluids), pro-

Bilateral

rhage), trauma, tumor, multiple sclerosis, encephali-

longed oral phase (pseudobulbar

 

tis, parkinsonism, multiple system atrophy, Alzheimer

palsy, akinesia, dysarthria, dys-

 

disease, Creutzfeldt–Jakob disease, hydrocephalus,

phonia, salivation, oromandibular

 

dystonia (toxic/drug-induced), chorea, intoxication,

dystonia)

 

cerebral palsy

Loss of swallowing reflex, im-

Brain stem,

Vascular lesions, multiple sclerosis, tumor, trauma,

paired pharyngeal phase, impaired

cerebellum

amyotrophic lateral sclerosis, syringobulbia, poliomy-

cough reflex (bulbar palsy, dy-

 

elitis, Arnold–Chiari malformation, central pontine

sarthria, respiratory disturbances),

 

myelinolysis, listerial meningitis, spinobulbar muscu-

risk of aspiration

 

lar atrophy, spinocerebellar degeneration

Weakness of muscles of mastica-

Cranial nerves

Facial paralysis, Guillain–Barré syndrome, diabetic

tion, impaired oral phase, im-

 

neuropathy, amyloidosis, base of skull syndrome

paired lip closure, nasal drip; im-

 

(p. 74)

paired pharyngeal phase (dy-

 

 

sarthria) may occur: depending on

 

 

which nerve/muscle is affected

 

 

Same as above (generalized my-

Neuromuscular

Myasthenia, amyotrophic lateral sclerosis, Lambert–

opathy, dysphonia)

 

Eaton syndrome, botulism, polymyositis/dermatomy-

 

 

ositis, scleroderma, hyperthyroidism, oculopharyn-

 

 

geal muscular dystrophy, myotonic dystrophy, facial–

scapular-humeral muscular dystrophy, nemaline myopathy, inclusion-body myositis

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