Ординатура / Офтальмология / Английские материалы / Clinical Neuro-ophthalmology A Practical Guide_Schiefer, Wilhelm , Hart_2007

Fig. 20.12. Acute-stage occlusion of the right posterior cerebral artery (arrows), diffusion-weighted image. This method images the earliest change during the development of an intracranial infarction, at between 1 and 2 h after the occlusion, transaxial tomographic plane

Invasive Angiographic Diagnosis

:Definition

Invasive angiography entails catheterization of the femoral artery, passage of the catheter into the vessels supplying the brain, and injection of iodinated contrast material. This approach is also used for the introduction of embolizing material (e.g., platinum coils) during invasive endovascular procedures.

The indications for invasive angiography include the diagnostic or the preinterventional study of a cerebrovascular malformation, such as an aneurysm, an arteriovenous malformation, or an arteriovenous fistula (■ Fig. 20.13). Endovascular closure by embolization is the treatment of choice for carotid–cavernous fistulas.

For a proven, acute obstruction of a central retinal artery, neuroradiologic intervention permits the direct intraarterial injection of fibrinolytic agents, which can be successful at restoring retinal circulation and vision up to about 6 h after onset of the infarction.

Fig. 20.13. a Lateral view, angiographic study of a traumatic ca- rotid–cavernous fistula (white arrow). Transmission of arterial pressure into the venous tree with marked enlargement of the superior ophthalmic vein (black arrow). b Lateral view, angiographic study of a traumatic carotid–cavernous fistula (thin arrow). After coil embolization (long arrow), angiogram shows closure of the fistula with restoration of proper orthograde blood blow in the intracranial arterial vessels (arrows in the upper half of the image)

Important Clinical Information Needed for Neuroradiologic Investigation

Clinical features that the neuroradiologist needs for proper investigation:

■The timing of onset, the course, and the duration neurologic disease

■A summary of the findings, including visual acuity, ocular motility, and visual field defects

■Suspected location (orbit, chiasm, cerebral cortex) and side of the lesion (right or left)

■Notes regarding any relative contraindication (allergies, renal insufficiency, cardiac pacemaker, metallic implants)

Conclusion

The strategic use of modern tomographic imaging, in conjunction with the clinical findings in neuro-ophthalmic disorders, provides a reliable means for efficient diagnosis. Interventional methods expand the range of potential diagnostic and therapeutic procedures through minimally invasive endovascular treatments for vascular occlusions or malformations.

Further Reading

Hosten N (1995) Auge und Orbita: Radiologische Differentialdiagnostik. Thieme, Stuttgart

Kretschmann H-J, Weinrich W (2002) Klinische Neuroanatomie und kranielle Bilddiagnostik. Thieme, Stuttgart

Radü E, Kendall B, Moseley I (1994) Computertomographie des Kopfes. Technische Grundlagen, Interpretation, Klinik, MRT-Zusatzinfor- mationen. Thieme, Stuttgart

Sartor K (1992) MR imaging of the skull and brain. A correlative text atlas. Springer, Berlin Heidelberg New York

Sartor K (1996) Neuroradiologie. Thieme, Stuttgart

History, Psychological Findings,

and Neuropsychological Disorders

At the start of every neurological examination, there should be at least a minimal attempt to take a history of the patient’s symptoms. This practice provides the physician with an opportunity to learn in general about the patient’s psychological state, including speaking and language disorders or other neuropsychological deficits. Other individual or isolated problems may be difficult to draw out and require a more targeted form of questioning.

Psychological State

• Pearl

The state of the patient’s awareness of his or her identity

Clues about the presence of a neurodegenerative disorder (for example, vascular encephalopathy with dementia and ocular motility disturbances, or Richardson-Steele-Olsze- wski syndrome with dementia and vertical gaze palsy) also help with assessing the reliability of the patient’s historical accounts.

Neuropsychological Disorders

Acquired neuropsychological disorders are, as a rule, the product of pathological events affecting the cerebral hemispheres. Most commonly, these are encountered in the setting of a recent stroke. Other potential causes include hemispheric tumors, head trauma, encephalitides, and neurodegenerative diseases.

Aphasia

:Definition

Aphasias are central nervous system (CNS) disorders that cause a change in or loss of the communicative use of language. Dysarthrias are different in that they are disorders of the motor functions of speech, i.e., problems of poor verbal articulation because of loss of motor control and/or of sensory feedback within the speaking apparatus.

Apraxia

:Definition

Apraxia is a central disturbance of sequences of movement and motor behaviors, despite retained motor function and coordination, mostly associated with lesions in the parietal lobes (■ Table 21.4; see also Chap. 13).

Important Signs and Symptoms (Tabulated)

nerve roots caused by prolapsed intervertebral discs.

Clinical Testing of Cranial Nerve Function

Isolated deficits in the function of individual cranial nerve can by caused by inflammatory (e.g., borreliosis, or idiopathic hemifacial paralysis [■ Fig. 21.1]) or by space-oc- cupying lesions like tumors or aneurysms. In addition, abrupt mononeuropathies of the cranial nerves that innervate the extraocular muscles is frequently encountered in patients with chronic metabolic disorders, such as diabetes (■ Table 21.5).

• Pearl

Clinically it is important to differentiate peripheral mononeuropathies of cranial nerves from disorders of cranial nerves associated with failures of other brainstem systems.

In addition to the central nuclei and the proximal portions of cranial nerves III through XII, which are arranged in descending order through the brainstem (mesencephalon, pons, medulla oblongata), are other important neural structures, all crowded closely together. Numerous afferents, including the dorsal columns, the spinothalamic, and the spinocerebellar pathways that connect the brain and the cerebellum with input from the spinal cord and efferent pathways (especially the pyramidal tract), all pass through this region, where many of them decussate to the contralateral side. Control of eye movements is organized in the

Fig. 21.1. Differential diagnosis of a facial palsy on the right side. a, b Peripheral facial palsy: a faulty lid closure with lagophthalmos and Bell’s phenomenon; the patient is additionally asked to look forced upwards b paralysis of the perioral musculature in company with paralysis of the temporal branch of the facial nerve; c, d central facial palsy – c normal lid closure, d paresis of the perioral muscles and superior facial symmetry

Reduced acuity, visual field defects, papilledema, optic disc pallor

Ocular muscle or gaze paresis, chooses eccentric gaze position, nystagmus, anisocoria

central (sparing the brow) or peripheral paresis (with Bell’s phenomenon)

See ■ Fig. 21.1

Nystagmus

:Definition

Nystagmus is an involuntary, rhythmic oscillatory movement, usually of both eyes. In a jerk nystagmus, a slower drift in eye position is countered by sequential, intermittent saccadic movements in the opposite direction. By convention, the direction of a nystagmus is named according to the direction of the fast phase.

Physiological forms of nystagmus include positional (end gaze) nystagmus, vestibular nystagmus, and optokinetic nystagmus (OKN). Pathological types of nystagmus are most commonly the result of disorders of the brainstem or cerebellum. A simplifying rule states that nystagmus without vertigo has a central cause, whereas the type that

caused by disease that lies outside of the CNS (■ Table 21.6; see Chap. 11).

Gaze Palsies

:Definition

Gaze palsies are supranuclear disturbances of conjugate movements of both eyes.

This implies that the extraocular muscles and their peripheral innervation, including the cranial nerve nuclei, are intact. The most important causes of gaze palsies are cerebral infarcts, multiple sclerosis, tumors, Wernicke’s encephalopathy, and neurodegenerative disorders, such as progressive supranuclear palsy (PSP) (■ Fig. 21.3, ■ Table 21.7; see

Most common form is that seen in internuclear ophthalmoplegia

Can be tested with an optokinetic drum or tape, pathological asymmetry found

with lesions of the temporoparietooccipital region (Area 19) see ■ Fig. 13.1

λPosterior medial longitudinal fasciculus (MLF) connecting the cranial nerve nuclei of the third and sixth cranial nerves (pontomesencephalic)

Frequently subtotal and evident as a visible slowing of saccadic velocity of the adducting eye

Frequently bilateral

eye on gaze to the right side. b Normal adduction during accommodative convergence, proving that the medial rectus itself is unaffected

Definition

Dysarthria is a disturbance of the motor control of speech, resulting in poor articulation.

In contradistinction to aphasia, which is categorized as a neuropsychological deficit (see above), dysarthria is a purely motor disturbance of the mechanics of speech. The understanding of language is unaffected, so communicais less severely affected by dysarthrias than it is by

aphasias (■ Table 21.8).

Clinical Testing of Motor Function

Tests of arm and leg positional stability provide a way of quickly detecting the presence of a motor deficit, as for example, following a suspected stroke (■ Fig. 21.4). Relatively subtle motor disturbances can be detected by this sort of testing, although it does not contribute much to a differential diagnosis of the source of the problem. In addition, peripheral pareses of individual nerves or nerve roots can sometimes be missed.

• Pearl

For a complete analysis of motor deficits, the positional stability tests should be augmented with attention to the signs of atrophy, the strengths of specific muscle groups, and the muscular tone of the neck and the extremities (■ Fig. 21.5, ■ Table 21.9).

Diagnostic conclusions about the location of damage can be drawn from the topical distribution of pareses. Therefore, for example, a hemiparesis immediately alerts the examiner to the presence of a central disorder (■ Fig. 21.6).

Additional clues for distinguishing between central and peripheral pareses are listed in ■ Table 21.10.