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Abnormalities of Smell
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Richard L. Doty, Steven M. Bromley
The neurological evaluation should focus on cranial nerve function, with particular attention to the optic nerve (CN II), trigeminal nerve (CN V), and the facial nerve (CN VII). Visual acuity, visual field, and optic disc examinations aid in the detection of possible intra-cranial mass lesions resulting in increased intra-cranial pressure (papilloedema) and optic atrophy, especially when considering Foster Kennedy syndrome (described below). General sensation over the face should be done (e.g., cotton, pin-prick, temperature). The nasal tickle, performed by using cotton to tickle the inside of one nostril, is also useful since an asymmetric withdrawal response suggests impairment of trigeminal fibres within the nose. The face should be symmetrical and full strength, with intact taste on the anterior two-thirds of the tongue bilaterally. Signs of frontal lobe injury and memory impairment may also aide in the diagnosis.
Anatomy for neurotrauma
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Essentials of Anesthesia for Neurotrauma, 2018
Vasudha Singhal, Sarabpreet Singh
The anterior cranial fossa supports the frontal lobes of the cerebral hemispheres. Its floor is formed by the orbital plate of the frontal bone; the cribriform plate (for passage of the olfactory nerve) and crista galli (for attachment of falx cerebri) of the ethmoid bone; and the lesser wings, planum sphenoidale, and prechiasmatic sulcus of the sphenoid bone. The olfactory tracts lie above the planum sphenoidale, while the optic chiasma usually lies above the prechiasmatic sulcus. Skull base fractures (Figure 2.1) in the region of the anterior cranial fossa may cause CSF rhinorrhoea, pneumocephalus, olfactory nerve damage leading to anosmia (due to damage to the cribriform plate), bilateral periorbital ecchymosis (Raccoon’s eyes), and damage to optic nerve and orbital contents. Frontal lobe injury leading to personality and behavioral changes may also occur in such fractures.
Topic 11 Consultation Liaison Psychiatry
Published in Melvyn W.B. Zhang, Cyrus S.H. Ho, Roger C.M. Ho, Basant K. Puri, Get Through, 2016
Melvyn W.B. Zhang, Cyrus S.H. Ho, Roger C.M. Ho, Basant K. Puri
Aetiological factors and severity of head injury Biological factors include the age at the time of the injury, the extent and the location of the brain injury, post-traumatic epilepsy.Psychological factors include premorbid personality, premorbid intelligence and psychological reactions to the injury.Social factors include premorbid social functioning, social support and mild head injury.In mild head injury, the Glasgow Coma scale (GCS) is between 14 and 15. Pay attention if the patient shows neurological signs: has haematoma, a history of coagulopathy, drug or alcohol consumption, epilepsy and past neurosurgery and is more than 60 years old.In moderate head injury, the GCS is 9–13. The mortality is less than 20%, although the morbidity is more than 50%. Positive neuroimaging finding in 40% of patients; 8% require neurosurgery.In severe head injury, the GCS is less than 9. Outcomes: It accounts for 10% of all head injuries, with a mortality of 40%.Post-concussion syndrome occurs after minor head injury. Post-concussion syndrome is associated with premorbid physical and social problems. It usually lasts from several weeks to 3 months and is more likely to be persistent in women. Common physical symptoms include headache, nausea and sensitivity to light and noise. Common psychological symptoms include cognitive impairment, poor concentration and irritability.Neuropsychiatric sequelae of frontal lobe injury: Frontal polar damage leads to poor judgement and insight, apathy and impaired problem solving. There is often no understanding of the impact of the disability on others. Orbitofrontal damage is associated with personality changes, impaired social judgement, impulsivity, hyperactivity, disinhibition, lability of mood, excitability and childishness or moria (childlike interest). Dorsolateral damage is associated with executive dysfunction, apathy, psychomotor retardation, preservation, poor initiation of tasks and memory impairment. Dorsolateral damageis associated with akinetic mutism. Left frontal lesion is associated with impairment in verbal recall.
Predictors and correlates of emotionalism across acquired and progressive neurological conditions: A systematic review
Published in Neuropsychological Rehabilitation, 2023
Sophie Fitzgerald, Fergus Gracey, Emma Trigg, Niall Broomfield
Furthermore, there was a considerable amount of research included in this review that supported the gate control theory highlighting the role of the cerebellum in the modulation of emotion and cerebellar pathways or lesions from the motor, frontal and temporal lobes to the brainstem (Parvizi et al., 2009). The research found individuals with emotionalism had increased mean diffusivity of white matter tracts underlying the frontotemporal cortex, the transverse pontine fibres and the middle cerebellar peduncle following a stroke (Floeter et al., 2014). Also, the left cerebellum posterior lobe was significantly lower for ALS individuals with emotionalism (Liu et al., 2017). Additionally, there was a greater frequency of frontal lobe injury and a difference in the frequency of frontal lobe lesions in individuals with emotionalism following a TBI (Tateno et al., 2004).
Spatial neglect treatment: The brain’s spatial-motor Aiming systems
Published in Neuropsychological Rehabilitation, 2022
A. M. Barrett, Kelly M. Goedert, Alexandre R. Carter, Amit Chaudhari
Our discovery that Aiming spatial neglect predicted functional recovery after receiving prism adaptation treatment led us to pursue a neuroanatomic predictor of prism adaptation response. We reasoned that neuroanatomic biomarkers may be a more feasible basis for spatial neglect treatment assignment than behavioural assessment, if the current clinical process is insensitive to spatial neglect features that predict response to prism adaptation treatment, since most patients receive brain imaging during clinical care. In the previous sections, we discussed the evidence that either frontal cortical injury, or disruption and disconnection of frontal-subcortical networks, may cause Aiming spatial neglect. Thus, we performed two studies of prism adaptation treatment for spatial neglect in which right brain stroke patients were screened for simple presence or absence of lesions anywhere in the frontal cortex (Chen et al., 2014; Goedert et al., 2020). In both of these studies, patients with frontal lesions responded better to prism adaptation treatment based on functional performance assessment with the CBS. The second study (Goedert et al., 2020) included control patients who did not receive prism adaptation therapy, to account for possible better recovery in frontal lobe-lesioned patients. Although both of these studies were small, and their results need to be confirmed before they can be broadly generalized, taken together they strongly suggest there is better response to prism adaptation therapy after frontal lobe injury.
Loss of smell in patients with traumatic brain injury is associated with neuropsychiatric behavioral alterations
Published in Brain Injury, 2021
Cristobal Langdon, Sara Laxe, Eduardo Lehrer, Joan Berenguer, Isam Alobid, Llorenç Quintó, Franklin Mariño-Sánchez, Montserrat Bernabeu, Concepció Marin, Joaquim Mullol
Finally, we found that 63% of the patients with olfactory dysfunction had a frontal head injury, which is in accordance with the findings of Fuji and coworkers (38); they reported that 83.3% of patients sustained either front or back injuries. Curiously, in our cohort a greater proportion of frontal lobe injury that was found in those without OI (74%). The fact that the olfactory bulb is located longitudinally in the olfactory sulcus and the central olfactory structures are just above this area makes them extremely susceptible to damage following a front to back TBI (3). According to several studies, there is a strong correlation between the severity of a trauma (as defined by GCS) with olfactory dysfunction (33). Both severe and moderate TBI are associated with olfactory dysfunction (39). In our study, the GCS score at the moment of the TBI was found to be lower for the NOD group compared to the OD group, indicating that patients with worse probable outcomes following a TBI report less olfactory deficits than those with a higher GCS. This is in accordance with studies that have shown that patients with a TBI are less aware of their olfactory deficit (25,40).