Medical Neurosciences 731 Afferent Home
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ACCESSORY CUNEATE NUCLEUS

You should recall from the spinal cord module that proprioceptive information from muscle spindles (Ia, II) and Golgi tendon organs (Ib) reaches the cerebellum via the dorsal spinocerebellar tract. The cells of origin of this tract lie in the ipsilateral Clarke’s column. This column of cells is present only at spinal cord levels C8L3. Central processes of dorsal root neurons that enter caudal to L3 have to ascend to reach L3. Consequently, Clarke’s column is quite enlarged caudally. (Clarke’s column neurons at L3 need to serve not only entering fibers at L3, but all of those entering below L3.)

Ia, Ib and type II axons of the dorsal root ganglia rostral to Clarke’s column (C8) pass rostrally to reach the ipsilateral caudal medulla, where they end within the ACCESSORY CUNEATE (“wedgeshaped”) NUCLEUS. This nucleus, which is somewhat difficult to see, lies dorsal to the spinal tract and nucleus V and lateral to the most rostral pole of nucleus cuneatus. Cells in the accessory cuneate nucleus send their axons to the IPSILATERAL CEREBELLUM via a fiber bundle called the INFERIOR CEREBELLAR PEDUNCLE (together with the dorsal spinocerebellar fibers). This pathway is called the CUNEOCEREBELLAR TRACT.

The accessory cuneate nucleus is concerned with relaying proprioceptive information from the arm (and neck) to the cerebellum, and the nucleus can be considered as the rostral equivalent of Clarke’s column.



REMEMBER: Accessory cuneate nucleus:
1). lies in the medulla.
2). receives UNCROSSED fibers from dorsal root ganglia above C8.
3). receives the same kind of information that Clarke’s column does.
4). projects to the IPSILATERAL cerebellum via inferior cerebellar peduncle.
5). is concerned with the arm, while Clarke’s column is concerned with the forearm, trunk and lower extremity.



Due to its small size, lesions restricted to the accessory cuneate nucleus are rare. Understanding the laterality (which side) and specific deficits resulting from a lesion of the accessory cuneate requires knowing something about CEREBELLAR functions and connections. While this important topic is covered later in this course, we need to do some limited spade work right now to get you prepared for those lectures, and also to let you problem solve on questions regarding lesions of brain stem areas that either project to the cerebellum (like the accessory cuneate nucleus, inferior olive and pontine grey [the latter two will be discussed further up the brain stem]) or contain axons leaving the cerebellum (superior cerebellar peduncle).

The cerebellum is involved in motor coordination. Unlike the cerebrum (i.e., cerebral cortex; cells of origin of the corticospinal tract), the cerebellum has no major projections to the spinal cord, but instead regulates movement indirectly by projecting to areas of the brain that do project upon the spinal cord. Lesions of the cerebellum lead to defects in the coordination of movements, but NOT paresis or paralysis. Such cerebellar defects involve errors in the rate, range or direction of voluntary movements. Disturbances following cerebellar lesions are known by a variety of terms such as nystagmus, ataxia, hypotonia, dysmetria, past pointing, rebound, dysdiadochokinesia, asynergy, intention tremor and decomposition of movement (WHEY!).

RIGHT NOW, LET’S JUST CALL THESE DISTURBANCES = INCOORDINATION/ATAXIA AND REMEMBER THAT INCOORDINATION/ATAXIA RESULTS FROM LESIONS OF THE CEREBELLUM OR ITS INPUTS (ACCESSORY CUNEATE NUCLEUS) OR OUTPUTS.

In addition to knowing that lesions of the cerebellum and its inputs and outputs result in incoordination, we need to know what part of the body is affected (arm, leg) and the laterality of the deficits (IPSI. or CONTRA.). The important point now is that one side of the cerebellum controls the SAME OR IPSILATERAL SIDE OF THE BODY.



OPTIONAL READING

This is due to TWO DECUSSATIONS of pathways involved in conveying cerebellar information to the spinal cord. To understand all of this, let’s start at the LEFT accessory cuneate nucleus, which you now know receives information from the LEFT side of the upper extremity. Cells in the LEFT accessory cuneate nucleus possess axons that comprise the LEFT cuneocerebellar tract and synapse on cells in the LEFT cerebellar cortex called granule cells. The axons of granule cells synapse on Purkinje cells. Purkinje cell axons synapse on cells in the deep white matter of the cerebellum called DEEP CEREBELLAR NUCLEI. There are four of these deep cerebellar nuclei on each side of the cerebellum. They are called fastigial, globose, emboliform and dentate. We will NOT worry about these nuclei too much at this time, but we need to know that they contain cells whose axons LEAVE the cerebellum (efferent; exit) in a large bundle called the SUPERIOR CEREBELLAR PEDUNCLE (Point #17). The superior cerebellar peduncle courses rostrally and CROSSES in the caudal midbrain (decussation #1). After crossing, axons synapse in the RED NUCLEUS (midbrain; we will discuss later in POINT #21; don’t worry about it at this time) and in the ventral lateral (VL) and ventral anterior (VA) nuclei of the thalamus. Cells in VL and VA project to the motor cortex, which of course contains the cells of origin of the CORTICOSPINAL TRACT. As you know, the corticospinal tract CROSSES in the caudal medulla (decussation #2) and innervates spinal cord neurons.





This leads to two of the most important “rules” of neurology. That is:CEREBELLAR PROBLEMS = IPSILATERAL, CEREBRAL PROBLEMS = CONTRALATERAL

The accessory cuneate nucleus projects to the IPSILATERAL CEREBELLAR HEMISPHERE (via the inferior cerebellar peduncle, along with the dorsal spinocerebellar fibers). Therefore lesions of the accessory cuneate nucleus, like the cerebellum, result in IPSILATERAL deficits. For example, the LEFT accessory cuneate nucleus receives input from Ia, Ib and type II fibers of dorsal root ganglia above C8 on the LEFT. The LEFT accessory cuneate nucleus projects to the LEFT cerebellar hemisphere. Finally the information leaves the cerebellum to eventually influence the LEFT arm. Therefore, a lesion of the LEFT accessory cuneate nucleus would result in “bad” information reaching the LEFT cerebellar hemisphere, and in turn motor incoordination of the LEFT arm. There is NO paralysis or atrophy of these muscles. REMEMBER, for our problem solving questions involving the accessory cuneate nucleus let’s just focus on INCOORDINATION/ATAXIA OF THE IPSILATERAL ARM.

To review: a lesion of the accessory cuneate nucleus results in incoordination/ataxia of the ipsilateral arm. It could not result in a Romberg because it involves a cerebellar afferent (and does not include the lower limbs anyway). A lesion of the DSCT will involve the legs but again, it is a cerebellar afferent and therefore would not give a Romberg sign. What about a lesion of the inferior cerebellar peduncle?



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