Susan’s main areas of difficulty involve motor speech, which affects her intelligibility. Particularly relating to the larynx, use of the tongue in speech and coordination of the lips and palate. This indicates that Susan is likely experiencing mixed spastic-ataxic dysarthria due to lesions on the upper motor neurone pathway (Wilkinson and Lennox 2005) in the corticobulbar tract which innervates the cranial nerves and the cerebellum (Bethoux et al 2013). Lesions on the upper motor neurone pathway/ corticobulbar tract would typically cause the spastic symptoms that the client is showing e.g. slower rate of speech, increased muscle tone and imprecise consonants (Weismer 2006) and lesions in the cerebellum would explain the ataxic dysarthria symptoms
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In this client it appears that the direct activation pathway, which is part of the upper motor neurone pathway (Wilkinson and Lennox 2005), will be affected including the cortico-bulba which supplies the speech mechanism. A lesion here will result increased spasticity (Duffy 2013) and will result in loss of skilled movement execution e.g. speech/ writing (Duffy 2013). Damage in the direct activation pathway will also affect the indirect activation pathway, which is also part of the upper motor neurone pathway (Wilkinson and Lennox 2005), as they are connected. Damage here will also cause spasticity (Duffy 2013) but will affect posture and increase muscle tone, this is evidenced in Susan’s symptoms. The cerebellum is also likely to be affected in this client. This is referred to as the cerebellar control circuit (Duffy 2013). Damage here can cause a lack of control and incoordination (Duffy 2013) such as the slow movement and slurred speech that is seen in …show more content…
The main nerves affected in dysarthria are the glossopharyngeal nerve (IX), vagus (X) and hyperglossal (XII), all three of these pairs of nerves originate in the medulla oblongata (Duffy 2013), which is an area of damage for Susan.
The glossopharyngeal nerve controls the posterior third of the tongue, part of the pharynx and the palate meaning it is important in the process of swallowing (Duffy 2013), which is starting to become affected in this client. Damage here would also explain the client’s presentation of slight hypernasality and occasional experience of water coming through her nose, as the palate sensation will be affected (Duffy 2013).
The vagus nerve has also been affected in this client. This nerve is responsible for motor control of the palate and part of the pharynx, including the larynx (Duffy 2013). An area of presentation relevant to this nerve damage is her aforementioned lack of consistent control of her palate, this can therefore affect resonance and articulation (Miller 2011). This nerve is also starting to affect Susan’s swallow. But Susan is also presenting with dysphonia or a ‘harsh sounding’ voice and the laryngeal exercises are the area she struggled with most on the Frenchay assessment. This indicates that innervation of the laryngeal muscles via the vagus nerve and its branches (superior laryngeal and recurrent laryngeal nerves) have been damaged by lesions and could subsequently be the cause
In this client it appears that the direct activation pathway, which is part of the upper motor neurone pathway (Wilkinson and Lennox 2005), will be affected including the cortico-bulba which supplies the speech mechanism. A lesion here will result increased spasticity (Duffy 2013) and will result in loss of skilled movement execution e.g. speech/ writing (Duffy 2013). Damage in the direct activation pathway will also affect the indirect activation pathway, which is also part of the upper motor neurone pathway (Wilkinson and Lennox 2005), as they are connected. Damage here will also cause spasticity (Duffy 2013) but will affect posture and increase muscle tone, this is evidenced in Susan’s symptoms. The cerebellum is also likely to be affected in this client. This is referred to as the cerebellar control circuit (Duffy 2013). Damage here can cause a lack of control and incoordination (Duffy 2013) such as the slow movement and slurred speech that is seen in …show more content…
The main nerves affected in dysarthria are the glossopharyngeal nerve (IX), vagus (X) and hyperglossal (XII), all three of these pairs of nerves originate in the medulla oblongata (Duffy 2013), which is an area of damage for Susan.
The glossopharyngeal nerve controls the posterior third of the tongue, part of the pharynx and the palate meaning it is important in the process of swallowing (Duffy 2013), which is starting to become affected in this client. Damage here would also explain the client’s presentation of slight hypernasality and occasional experience of water coming through her nose, as the palate sensation will be affected (Duffy 2013).
The vagus nerve has also been affected in this client. This nerve is responsible for motor control of the palate and part of the pharynx, including the larynx (Duffy 2013). An area of presentation relevant to this nerve damage is her aforementioned lack of consistent control of her palate, this can therefore affect resonance and articulation (Miller 2011). This nerve is also starting to affect Susan’s swallow. But Susan is also presenting with dysphonia or a ‘harsh sounding’ voice and the laryngeal exercises are the area she struggled with most on the Frenchay assessment. This indicates that innervation of the laryngeal muscles via the vagus nerve and its branches (superior laryngeal and recurrent laryngeal nerves) have been damaged by lesions and could subsequently be the cause