Approach to DBS in the Vicinity of the Subthalamic Nucleus

The regional anatomy around the DBS lead in the subthalamic nucleus (STN) determines efficacy and adverse effects. Understanding the regional anatomy allows the programmer to adjust the stimulation to provide optimal benefit and the absence of adverse effects.The STN lies near the junction of the diencephalon and mesencephalon. It is just ventral to the thalamus, just lateral to the brachium conjunctivum and red nucleus, and medial and dorsal to the internal capsule. These structures are important because inappropriate stimulation causes side effects. For examples: Electrical fields spreading to ascending sensory medial lemniscus and spinothalamic pathways behind the STN produce paresthesias. Inadvertent stimulation of the brachium conjunctivum can cause ataxia and loss of balance. The red nucleus lies in the brachium conjunctivum, and the exiting axons from the oculomotor nucleus run within the red nucleus. Electrical fields spreading to these structures can result in disconjugate gaze and diplopia. Stimulating the internal capsule laterally or dorsally can cause tonic muscle contractions.

The Dentato-Rubro-Olivary Tract: Clinical Dimension of This Anatomical Pathway

Symptomatic palatal tremor is potentially the result of a lesion in the triangle of Guillain-Mollaret (1931) and is associated with hypertrophic olivary degeneration (HOD) which has characteristic MR findings. The triangle is defined by dentate efferents ascending through the superior cerebellar peduncle and crossing in the decussation of the brachium conjunctivum inferior to the red nucleus, to finaliy reach the inferior olivary nucleus (ION) via the central tegmental tract. The triangle is completed by ION decussating efferents terminating on the original dentate nucleus via the inferior cerebellar peduncle. We can demonstrate the anatomy of this anatomical triangle using a clinical case of palatal tremor presenting with bilateral subjective pulsatile tinnitus along with the pathognomonic MR findings previously described. The hyperintense T2 signal in these patients may be permanent, but the hypertrophied olive normally regresses after 4 years. The temporal relationship between the evolution of the histopathology and the development of the palatal tremor remains unknown as does the natural history of the tremor. Botox injection at the level of tensor and levator veli palatini insertion have been used to treat patients with disabling tremor synchronous tinnitus. A lesion involving the triangle can have a quite varied clinical expression.

A Medley of Midbrain Maladies: A Brief Review of Midbrain Anatomy and Syndromology for Radiologists

The midbrain represents the uppermost portion of the brainstem, containing numerous important nuclei and white matter tracts, most of which are involved in motor control, as well as the auditory and visual pathways. Notable midbrain nuclei include the superior and inferior colliculus nuclei, red nucleus, substantia nigra, oculomotor nuclear complex, and trochlear nucleus. In addition, white matter tracts include the brachium conjunctivum, medial and lateral lemniscus, spinothalamic tracts, and the fiber tracts within the cerebral peduncles. Although neurologically vital, many of these small midbrain nuclei and white matter tracts are not easily individually identified on neuroimaging. However, given their diverse functions, midbrain pathology often leads to distinct clinical syndromes. A review and understanding of the location and relationships between the different midbrain nuclei and fiber tracts will allow more precise correlation of radiologic findings with patient pathology and symptomatology. Particular syndromes associated with midbrain pathology include the Weber, Claude, Benedikt, Nothnagel, and Parinaud syndromes. The oculomotor and trochlear cranial nerves also reside at this level. An understanding of their functions as well as their projected courses from the midbrain towards the eye allows identification of distinct locations which are particularly vulnerable to pathology.

Conditioned Eyeblink Response Consists of Two Distinct Components

The aim of these experiments was to obtain a detailed knowledge of how the orbicularis oculi muscle is activated during the execution of a conditioned eyeblink response (CR). This is the first critical step to understand the underlying neural mechanisms involved in the control of the CR. Decerebrate ferrets were trained in a classical conditioning paradigm. The conditioned stimulus (CS) was a train of electrical stimuli (15 pulses, 50 Hz, 1 mA) applied to the forelimb, and the unconditioned stimulus (US) was a train of electrical stimuli (3 pulses, 50 Hz, 3–4 mA) to the periorbital region. The CRs were studied by recording electromyograms (EMGs) from the orbicularis oculi muscle. The eyeblink CR in all animals showed a similar topography with at least two different components, CR1 and CR2, which were expressed at different rates. CR1 appeared first during acquisition, had a shorter onset latency, and was more phasic and more resistant to extinction than CR2. A marked pause in the muscle activity separated the two components. To control that the two-component CR were not species, paradigm or preparation specific, awake rabbits were trained with a tone CS (300 ms, 4 kHz, 64 dB) and a train of periorbital stimuli as US (3 pulses, 50 Hz, 3 mA). CR1 and CR2 were present in the rabbit eyeblink CR. The cerebellum is implicated in the control of CRs and to study whether separate neural pathways were responsible for CR1 and CR2, direct brachium pontis stimulation was used to replace the forelimb CS. CR1 and CR2 were present in the CR elicited by the brachium pontis CS. The presence of CR1 and CR2 after a unilateral lesion of the brachium conjunctivum shows that output from the contralateral cerebellar hemisphere was not the cause for any of the components. Other mechanisms that might be involved in the separation of the CR into two components are discussed. The results show that the eyeblink CR consists of at least two components, CR1 and CR2, which most likely originate either as a direct central command from the cerebellum or in the output pathway before the facial nucleus.

Cerebellar and cerebral inputs to corticocortical and corticofugal neurons in areas 5 and 7 in the cat

1. In the parietal cortex (Px, areas 5 and 7), the organization and characteristics of cerebellar and cerebral inputs and their effects on efferent neurons were investigated with the use of intracellular and extracellular recording techniques in the anesthetized cat. 2. Evoked field potential analysis revealed that two regions of the Px, the caudal bank of the ansate sulcus (Ans. S.) and the crown of the suprasylvian gyrus (Ssyl. G.), received converging input from the dentate and the interpositus nucleus. The cerebellar input to the caudal bank of the Ans. S. was relayed via the ventrolateral region of the ventroanterior-ventrolateral (VA-VL) complex of the thalamus, whereas the cerebellar input to the crown of the Ssyl. G. was relayed via the dorsomedial region of the VA-VL complex. 3. A total of 176 neurons was recorded intracellularly in the Px to examine inputs from the cerebellum. Of these, 72 neurons were corticocortical neurons projecting to the motor cortex (Mx), and 48 were corticofugal neurons to the pontine nucleus (PN). Intracellular staining with horseradish peroxidase revealed that the former corticocortical neurons were layer III pyramidal neurons and the latter corticofugal neurons were layer V pyramidal neurons. 4. Stimulation of the brachium conjunctivum (BC) produced di- or polysynaptic excitatory postsynaptic potentials (EPSPs) in corticocortical neurons projecting to the Mx and corticofugal neurons to the pontine nucleus in the Px. The characteristics of BC-evoked EPSPs were different between the bank of the Ans. S. and the crown of the Ssyl. G. In the bank of the Ans. S., the slope of the rising phase of the BC-evoked EPSPs was steeper, and their minimum latency was shorter by 0.8 ms than those in the crown of the Ssyl. G. These differences may reflect differences in the terminal distribution and conduction velocity of the thalamocortical fibers relaying cerebellar input to these two parietal areas. 5. Stimulation of the Mx produced mono- or disynaptic EPSPs in both corticocortical neurons projecting to the Mx and corticofugal neurons projecting to the pontine nucleus in the Px. For each neuron, effective sites for inducing EPSPs were distributed very widely and sometimes covered both areas 4 and 6. Extensive corticocortical projection from the Mx to the Px was confirmed by injection of an anterograde tracer into the Mx. 6. These data indicate that neurons in the Px receive inputs from both the cerebellum and the Mx and send outputs to the Mx and the cerebellum.(ABSTRACT TRUNCATED AT 400 WORDS)

Relative contributions of thalamic reticular nucleus neurons and intrinsic interneurons to inhibition of thalamic neurons projecting to the motor cortex

1. Intracellular responses to stimulation of the cerebral cortex (Cx) and cerebellum were analyzed in thalamocortical neurons (TCNs) in the ventroanterior-ventrolateral (VA-VL) complex of the thalamus and neurons in the thalamic reticular nuclei (RNs) of anesthetized cats, and the contribution of reticular nucleus neurons (RNNs) and thalamic interneurons (TINs) to cerebral and cerebellar inhibition of TCNs was determined. 2. Single TCNs projecting to area 4 or 6 received convergent monosynaptic excitatory and disynaptic inhibitory inputs from both the dentate nucleus (DN) and the interpositus nucleus (IN). These TCNs also received monosynaptic excitatory postsynaptic potentials (EPSPs) and disynaptic inhibitory postsynaptic potentials (IPSPs) from the pericruciate cortex (areas 4 and 6). Each TCN received the strongest excitatory and inhibitory inputs from the cortical area to which that TCN projected, and weaker inhibitory inputs from adjacent cortical areas. 3. RNNs were identified morphologically by intracellular injection of horseradish peroxidase (HRP). Stimulation of the brachium conjunctivum (BC) evoked disynaptic EPSPs with a long decay phase in RNNs in the anterior ventrolateral part of the RN. Single RNNs received convergent disynaptic excitatory inputs from both the DNA and the IN. Stimulation of the Cx produced monosynaptic long-lasting EPSPs with two different latencies in these RNNs: early EPSPs with latencies of 0.9-2.1 ms and late EPSPs with latencies of 1.8-3.5 ms. Collision experiments with BC- and Cx-evoked EPSPs in RNNs indicated that BC-evoked disynaptic EPSPs and Cx-evoked early EPSPs were produced by axon collaterals of TCNs to RNNs. The latencies of the Cx-evoked late EPSPs in RNNs were almost identical to those of Cx-evoked monosynaptic EPSPs in TCNs, indicating that corticothalamic neurons (CTNs) exert monosynaptic excitatory effects on RNNs and TCNs. 4. Stimulation of the Cx produced IPSPs in TCNs with short latencies of 1.8-2.7 ms and longer latencies of > or = 2.8 ms. The Cx-evoked early IPSPs with latencies of 1.8-2.7 ms were mediated by RNNs. The origin of Cx-evoked late IPSPs with latencies of > or = 2.8 ms in TCNs was twofold, Cx-induced early IPSPs in TCNs were facilitated by conditioning cortical stimulation that induced late IPSPs in the TCNs. The same conditioning cortical stimulation also facilitated BC-evoked disynaptic IPSPs. The time course of this facilitatation indicated that CTNs produce long-lasting excitation in TINs. These results indicated that Cx-evoked IPSPs with latencies of > 2.7 ms were mediated at least in part by RNNs and inhibitory TINs in the VA-VL complex.(ABSTRACT TRUNCATED AT 400 WORDS)