Section III Examination, Imaging, and Monitoring for Brainstem Surgery

10.1055/b-0039-173898

7 Neurologic Examination of the Brainstem and Thalamus

Yazan J. Alderazi and Mohamed S. Teleb

Abstract

The neurologic examination of the brainstem and the thalamus is rapid, informative, inexpensive, and clinically useful. The examination is central to lesion localization, determining the extent of neurologic dysfunction, prognostication, monitoring of patients for potential deterioration, monitoring of patients’ recovery, and planning treatment and rehabilitation strategies. We explore the components of the neurologic examination as they apply to the brainstem and thalamus. A practical, clinically oriented approach to lesion localization is presented. We provide useful heuristics and mnemonics to aid rapid patient assessment. A summary of thalamic syndromes and typical vascular brainstem syndromes is presented.

Introduction

The examination of the brainstem and thalamus is necessary for lesion localization, determining the extent of neurologic dysfunction, prognostication, monitoring of patients for potential deterioration, monitoring of patients’ recovery, and planning treatment and rehabilitation strategies. Although improved access to neuroimaging has undoubtedly improved our diagnostic capabilities, the neurologic examination is necessary and more useful for most of these tasks.

The examination of the brainstem and thalamus can be a difficult task (see Table 7.1 and Table 7.2 for lists of common lesions afflicting the brainstem and thalamus). The presentation is not always classic and can be a combination of different syndromes, affecting multiple cranial nuclei and numerous tracts (e.g., sensory, oculomotor, parasympathetic, and sympathetic). We review the basic examination steps, examine the most well-known stroke syndromes, and reveal multiple heuristics and shortcuts for localization. We emphasize anatomy and vascular supply, as appropriate.

**Table 7.1** Common brainstem syndromes
Classical name	Symptoms	Location or structures	Vascular supply
Dejerine syndrome (medial medullary syndrome)	Ipsilateral Hypoglossal nerve (CN XII) palsy Contralateral Hemiparesis; vibration and proprioception sensory loss; variable manifestations (e.g., isolated hemiparesis, tetraparesis, hemiparesis, ataxia, vertigo, nystagmus, dysphagia, facial palsy)	Hypoglossal nerve (CN XII) Corticospinal tract (in the pyramid); medial lemniscus	Vertebral artery: anteromedial artery Anterior spinal artery: anteromedial artery
Wallenberg syndrome (lateral medullary syndrome)	Ipsilateral Facial pain; facial sensory loss Ataxia (arm, leg, and gait at times) Nystagmus; nausea; vomiting; vertigo Hoarseness; dysphagia Horner syndrome Contralateral Hemisensory loss of pain and temperature sense Nonlateralized Hiccups	Trigeminal nerve (CN V) nucleus Restiform body; cerebellum Vestibular nucleus Nucleus ambiguous Descending sympathetic tracts Spinothalamic tract	Vertebral artery: distal branches Vertebral artery: superior lateral medullary artery Posterior inferior cerebellar artery: less common than vertebral artery
Foville syndrome (inferior medial pontine syndrome)	Ipsilateral Entire face weakness; lateral gaze palsy Contralateral Hemiparesis	Dorsal pontine tegmentum; caudal pons Facial nerve (CN VII) nucleus/fascicle; PPRF or abducens nerve (CN VI) nucleus; corticospinal tract	Basilar artery: paramedian branches Basilar artery: short circumferential arteries
Marie-Foix syndrome (lateral pontine syndrome)	Ipsilateral Ataxia (arm and leg) Contralateral Hemiparesis; variable hemisensory loss of pain and temperature sense	Corticopontine cerebellar tracts Corticospinal tracts Spinothalamic tract	Basilar artery: long circumferential branches Anterior inferior cerebellar artery
Raymond syndrome (ventral pontine syndrome; Raymond- Cestan-Chenais syndrome; alternating abducens hemiplegia)	Ipsilateral Lateral abduction (lateral rectus) palsy Contralateral Hemiparesis	Abducens nerve (CN VI) fascicle; pyramidal tract	Basilar artery: paramedian branches
Millard-Gubler syndrome (ventral pontine syndrome)	Ipsilateral Entire face weakness; lateral abduction (lateral rectus) palsy Contralateral Hemiparesis	Basis pontis (pyramidal tract); abducens nerve (CN VI) fascicle; facial nerve (CN VII) fascicle	Basilar artery: short circumferential branches Basilar artery: paramedian branches
Weber syndrome	Ipsilateral Lateral gaze weakness Contralateral Hemiparesis (upper and lower extremities)	Midbrain: base Oculomotor nerve (CN III) Corticospinal tract	Posterior cerebral artery: penetrating branches to midbrain
Benedikt syndrome	Ipsilateral Oculomotor nerve (CN III) palsy Contralateral Hemiparesis; involuntary movements (e.g., chorea, athetosis); tremor	Paramedian midbrain syndrome Oculomotor nerve (CN III) Cerebral peduncle; red nucleus; substantia nigra	Posterior cerebral artery: penetrating branches to midbrain
Claude syndrome	Ipsilateral Oculomotor nerve (CN III) palsy Contralateral Ataxia; cerebellar outflow tremor; hemiparesis (upper and lower extremities)	Midbrain Brachium conjunctivum, including dentato-rubro-thalamo-cortical tract Tegmentum Red nucleus Cerebral peduncle (corticospinal tract)	Posterior cerebral artery
Nothnagel syndrome (dorsal midbrain syndrome)	Ipsilateral Oculomotor nerve (CN III) palsy; ataxia; nystagmus Contralateral Oculomotor nerve (CN III) palsy (less severe); ataxia	Superior and inferior colliculi	Usually not vascular; neoplasms are common etiology
Anton syndrome	Cortical blindness; unawareness or denial of blindness	Cerebral hemisphere: bilateral occipital lobes	Posterior cerebral artery: bilateral Basilar artery: tip of basilar artery
Abbreviations: CN, cranial nerve; PPRF, paramedian pontine reticular formation.

**Table 7.2** Common Thalamic Syndromes
Classical name	Symptoms	Location or structures	Vascular supply
Anterior thalamic syndrome	Decreased level of consciousness; impaired memory, impaired executive function, abulia; hemispatial neglect (right-sided lesions)	Anterior nucleus and ventral anterior nuclei of the thalamus; mammillothalamic tract; amygdalofugal pathway	Tuberothalamic artery(arises from middle third of posterior communicating artery)
Paramedian thalamic syndrome	Decreased level of consciousness; memory impairment, cognitive impairment, and disinhibition; thalamic aphasia (left)	Dorsomedial nucleus; centromedian nucleus	Paramedian arteries(arising from P1 segment) Artery of Percheron variant (a single artery supplying bilateral paramedian arteries)
Inferolateral thalamic syndrome	Contralateral Hemisensory loss; hemiataxia; hemiparesis; hemianopia (involving the macula); postlesional thalamic pain syndrome with hemibody pain	Ventral posterior nuclei (lateral VPL, medial VPM, and inferior VPI); ventrolateral nucleus; medial geniculate body	Inferolateral arteries(arises from P2 segment)
Posterior thalamic syndrome	Homonymous hemianopia; homonymous quadrantanopia; aphasia (left-sided lesions); variable dystonia or sensory loss	LGN; pulvinar; midbrain; subthalamic nucleus	Posterior choroidal arteries(arises from P2 segment); lateral and medial choroidal artery branches
Abbreviations: LGN, lateral geniculate nucleus; VPI, ventral posterior inferior; VPL, ventral posterolateral; VPM, ventral posteromedial.

The brainstem is organized into three parts: the midbrain, pons, and medulla. In addition the thalamus, cerebellum, and spinal cord are adjacent structures in the central nervous system with tracts flowing in and out of the brainstem. The key to localization remains a good neurologic examination and understanding of functional neuroanatomy. Lesion localization requires all the aspects of a neurologic examination, including mental status, cranial nerve (CN) examination, motor examination, sensory examination, coordination assessment, and ataxia assessment. An efficient clinical assessment requires two steps: lesion localization, followed by etiologic differential diagnosis. Lesion localization is the requisite first step, as this allows a differential diagnosis focused on the most likely pathologies in the affected area. For example, the list of conditions affecting the pons is different from the list of those affecting the thalamus.

Examination

Mental Status

The mental status examination involves two parts: (1) assessment of the level of consciousness, and (2) assessment of the cognitive domains—language, memory, attention, and praxis—as well as testing for agnosia. The patient’s level of consciousness should be assessed using verbal, tactile, and painful stimuli, as necessary. The level of consciousness can be graded in unambiguous terms of decreasing consciousness: (1) awake and alert; (2) awake and lethargic; (3) stuporous or obtunded; and (4) comatose. Decreased level of consciousness indicates dysfunction of the reticular activating system, the thalamus, or the bilateral cerebral hemispheres. The so-called “structural causes” of coma—brainstem or thalamic infarction, and hemorrhages or mass lesion—are often responsible for this dysfunction. Structural causes must be distinguished from nonstructural causes of coma, which are essentially a severe manifestation of toxic-metabolic encephalopathy. Encephalopathy is a disorder of consciousness that is characterized by inattention, lethargy, or, in severe cases, stupor and coma. Encephalopathy is usually mediated by nonstructural causes, such as sodium imbalance, hypoglycemia, renal failure, liver failure, and hypercapnia, and it can lead to nonstructural coma in severe cases. The key distinction is that structural causes affecting the brainstem will also usually result in CN dysfunction, affecting ocular motility and pupil symmetry in particular.

A screening assessment of higher cortical functions is necessary because aphasia, agnosia, neglect, inattention, visual disturbances, visual field defects, and memory impairment may all indicate thalamic injury. These symptoms are more commonly caused by lesions in the cortical structures, but they can be caused by thalamic lesions.

The thalamus has reciprocal connections with the various structures within the frontal, parietal, temporal, and occipital lobes. ¹ ^, ² These connections include the primary and associative cortices. In addition, the thalamus has relays to the limbic system and the cerebellum. Through these connections, thalamic lesions may mimic cortical or cerebellar lesions and may also cause psychiatric manifestations such as mania, depression, and psychosis. ³ Thalamic aphasia with left thalamus lesions, thalamic neglect with right thalamus lesions, abulia due to anterior thalamic lesions, coma due to bilateral paramedian thalamic lesions, and contra-lateral ataxia due to ventral thalamic lesions are all examples of dysfunction of distant brain areas caused by failure of the functional network. ⁴ ^, ⁵ ^, ⁶ ^, ⁷ This dysfunction of distant areas is referred to as diaschisis and is typical of thalamic lesions. In addition, bilateral paramedian thalamic lesions can cause vertical gaze palsy. ⁸

Cranial Nerves

Examination of the CNs is necessary when evaluating oculomotor, sensory, and motor function. Specifically, CN dysfunction is an important clue to the presence of brainstem dysfunction. It is also the most reliable clinical method of determining the location of dysfunction within the brainstem: midbrain, pons, or medulla. ⁹

CN I: Olfactory Nerve

The olfactory nerve and sense of smell are rarely tested. However, test results can indicate a mass lesion in the anterior cranial fossa or some early neurodegenerative conditions such as Alzheimer disease. Testing the olfactory nerve is of no localization value for lesions of the brainstem and thalamus.

CN II: Optic Nerve

There are four components to the optic nerve examination: (1) visual acuity, (2) visual fields, (3) pupillary responses, and (4) funduscopy. Decreased visual acuity may localize to the optic nerve and the retina, or it may represent refractive error and thus not localize to the brainstem or thalamus. Thalamic lesions can cause visual field defects, namely, homonymous quadrantanopia or macular-sparing homonymous hemianopia, with damage to the lateral geniculate body. Rarely, lateral genicular nucleus lesions can cause macular-involving homonymous hemianopia, if damage is complete. This can occur in an interruption of the dual supply to the macular connections in the lateral geniculate body. Anisocoria (i.e., unequal pupils) indicates impaired balance between parasympathetic and sympathetic input into the pupil. Dilation of the impaired pupil (i.e., mydriasis) represents loss of parasympathetic input. This occurs in dysfunction of the efferent limb of the pupillary response, namely, damage to the midbrain, the oculomotor nerve (CN III) nucleus, the CN III within or external to the brainstem, or damage to the Edinger-Westphal nucleus within the midbrain. Alternatively, loss of pupillary sympathetic input causes constriction of the pupil (i.e., miosis). Miosis is part of Horner syndrome, which is also characterized by partial ptosis and anhidrosis. Pupillary constriction may indicate dysfunction of the sympathetic nervous system within the brainstem, and it may be particularly important for identifying lateral medullary lesions or damage to the sympathetic system outside the brainstem (e.g., within the hypothalamus, the spinal cord, or the sympathetic chain or along the carotid artery). Funduscopy is uncommonly abnormal for lesions of the brainstem or the thalamus; however, it may demonstrate papilledema in cases of concomitantly raised intracranial pressure, or it may demonstrate findings of underlying etiology in patients with hypertensive or diabetic retinopathy.

CN III: Oculomotor Nerve

CN III function is examined during testing of ocular movements, first by asking the patient to visually follow an “H” pattern made by the examiner’s finger movements and then by examining the pupillary responses. The oculomotor nerve controls eye motion, and the parasympathetic portion of the nerve controls pupillary response. The nerve may be damaged within the brainstem or along its extra-axial course to the extraocular muscles. Third nerve palsy is usually classified as CN III palsy involving the pupil when the pupil is dilated and as pupil-sparing CN III palsy when there is normal pupil function. CN III palsy involving the pupil usually indicates compressive lesions such as aneurysms (particularly those of the posterior communicating artery), tumors, or inflammatory mass lesions. Such is the case because compressive lesions interrupt both the oculomotor fibers supplying the extraocular muscles and the parasympathetic fibers supplying the pupil. Pupil-sparing CN III palsy occurs with noncompressive lesions, in particular with microvascular infarction of the nerve due to small vessel disease in patients with diabetes mellitus or hypertension. Infarction damages the inner nerve fibers supplying the extraocular muscles but spares the outer nerve fibers supplying parasympathetic control. In older terminology, impaired ocular motility is referred to as external ophthalmoplegia and pupillary dysfunction is referred to as internal ophthalmoplegia.

In an examination of ocular motility, the eye demonstrates ptosis and disconjugate movement in the primary position. Ptosis may be complete or incomplete, depending on the severity of dysfunction. The same is true for impaired ocular motility. The affected eye is “down-and-out” (i.e., inferiorly and laterally deviated due to unopposed actions of superior oblique and lateral rectus muscles). Adduction and supraduction are weak. In an examination of a patient with anisocoria, it is important to determine whether the dysfunction is in the constricted pupil, indicating Horner syndrome, or in the dilated pupil, indicating CN III palsy or a midbrain lesion. Diplopia occurs with CN III palsy but not with isolated Horner syndrome. The oculomotor nerve may be damaged anywhere along its course from the mid-brain to the subarachnoid space, the lateral wall of the cavernous sinus, the superior orbital fissure, or the extraocular muscles.

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