Cerebral peduncle

Fig. 5. The plate illustrates the ventral midbrain tegmentum as illustrated in the atlas of the rat brain of Swanson (1992), at levels approximately equivalent to those shown in Fig. 4. B and D are images of Nissl-stained sections. Abbreviations CLI, central linear nucleus of the raphe cpd, cerebral peduncle DGlb, dentate gyrus, lateral blade EW, Edinger-Westphal nucleus fr, fasciculus retroflexus hf, hippocampal fixure IF, interfascicular...

On the other hand, neurons in the most ventral part of the SNr were seen to give off dendrites oriented parallel to the cerebral peduncle. 

Fig. 12. The diagram, redrawn from Fallon and Loughlin (1995), summarizes the distribution in the rat of midbrain dopaminergic neurons which give origin to different sets of telencephalic projections. Abbreviations CP, cerebral peduncle ml, medial lemniscus MT, medial terminal nucleus of the accessory optic tract SNc, substantia nigra, pars compacta SN1, substantia nigra, pars lateralis SNr, substantia nigra, pars reticulata VTA, ventral tegmental area.

Fig. 5.1. Brain CT images showing a large hypodense (arrows) edematous cerebral infarct in the distribution of the middle cerebral artery, with midline shift. Such large infarcts cause herniation of the cingulate gyrus under the falx cerebri of the ispsilateral uncus under the tentorium to compress the oculomotor nerve, posterior cerebral artery and brainstem and of the contralateral cerebral peduncle to cause ipsilateral hemiparesis.

Lacunar syndromes are defined clinically. They are highly predictive of small, deep lesions affecting the motor and/or sensory pathways in the corona radiata, internal capsule, thalamus, cerebral peduncle or pons. Although a few patients have a partial anterior circulation infarct (Bamford et al. 1987 Anzalone and Landi 1989 Arboix et al. 2007), the great majority have small iirfarcts, which are sometimes visible on CT, more often on MRI. These are caused by presumed occlusion of a small perforating artery affected by intracranial small vessel disease (see Fig. 10.2). There is no visual field defect, no new cortical... 

Pure motor stroke constitutes about 50% of lacunar cases. It consists of a unilateral motor deficit involving two or three areas, the face, upper arm and/or leg, including the whole of each area that is affected. There are often sensory symptoms but no sensory signs. The lesion occurs at locations where the motor pathways are closely packed together and separate from other pathways usually in the internal capsule or pons, sometimes the corona radiata or cerebral peduncle, and rarely in the medullary pyramid. There may be a flurry of immediately preceding TIAs, the so-called capsular warning syndrome (Donnan et al. 1996). 

Ataxic hemiparesis constitutes about 10% of cases. It is the combination of corticospinal and ipsilateral cerebellar-like dysfunction affecting the arm and/or leg. It includes a syndrome in which there is little more than dysarthria and one clumsy hand. The lesion is usually in the pons, internal capsule or cerebral peduncle. Dysarthria, with or without upper motor neuron facial weakness, may also be a lacunar syndrome with similar lesion localization as ataxic hemiparesis, but there are other localizing possibilities as well. 

Fig. 17. A-D) Drawings of examples of individual substantia nigra pars reticulata neurons from sagittal sections. Neurons A-C are located in the dorsal part of the pars reticulata and show the typical pattern of dendrite spread that extends in the rostral-caudal dimension of the nucleus. The local axon collateral of neuron C is shown. Neuron D is located in the region of the pars reticulata adjacent to the cerebral peduncle in the ventral part of the nucleus. Neurons A, B and D are redrawn from Golgi impregnated neurons from Grofova et al. 1980. Neuron C is from an example provided by J. Tepper.

Fig. 6.6 WaUerian degeneration. Coronal T2 weighted image shows encephalomalacia of the right frontal and temporal lobes and T2 high signal extending into the right cerebral peduncle (arrow) from WaUerian degeneration...

Fig. 5.14. Right temporal lobe intracerebral hemorrhage due to a ruptured MCA aneurysm. Beside basal subarachnoid hemorrhage CT reveals brain edema, compression of the basal cisterns and the cerebral peduncle...

The authors explained the ipsilateral hemiparesis by invoking the Kernohan-Woltman notch phenomenon, in which intracranial mass lesions compress the cerebral peduncle on the opposite side against the tentorial notch, interrupting the fibers of the cerebrospinal tract. The subdural hematoma was aspirated and she was discharged with minimal weakness of the right leg. 

A relationship between substantia nigra lesions, striatal DA and movement disturbance was demonstrated by making unilateral lesions in the ventromedial tegmentum of the upper brain stem. This caused loss of cells in the substantia nigra, decrease of striatal DA and NA but not 5HT and contralateral hypokinesis [130, 131]. If lesions were made in dorsomedial fibres of the cerebral peduncle then striatal 5HT decreased [132]. Lesions of the above types cause not only depletion of the amines but also of the enzymes necessary for their synthesis, tyrosine hydroxylase, tryptophan hydroxylase and aromatic amino acid decarboxylase [133, 134]. 

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