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Techniques
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
The skull should be opened along the sutures. This exposes the brain, the removal of which is aided if performed under water so that it can ‘float’. Fixation can be accelerated using 20 per cent formalin in a 37°C oven for 2–3 days before section if return to the body is necessary. In cases of any posterior cranial fossa abnormality, a posterior approach is recommended (see also Chapter 15).
Choroid Plexus Tumors and Meningiomas
Published in David A. Walker, Giorgio Perilongo, Roger E. Taylor, Ian F. Pollack, Brain and Spinal Tumors of Childhood, 2020
Kenneth K. Wong, Elwira Szychot, Jennifer A. Cotter, Mark Krieger
Classically, symptoms may vary widely, depending upon the location of the mass. Lesions in the cerebellopontine angle may present with symptoms of cranial neuropathy, such as loss of hearing. Cerebral convexity meningioma may present with symptoms of headache or a seizure. Meningiomas of the sphenoid wing or optic nerve may be associated with visual loss. Visual field defects may be caused by parasellar meningiomas. Mild weakness of extraocular movements has been associated with cavernous sinus meningiomas. Compression of the olfactory tract by olfactory groove or sphenoid ridge meningiomas can cause anosmia. Mental status changes with apathy and inattention may result from large subfrontal or sphenoid ridge meningiomas. Large tumors of the posterior cranial fossa can cause obstructive hydrocephalus, and can present with papilledema and classic early-morning headache. Extremity weakness can be a presenting symptom due to meningiomas at different sites. A parasagittal meningioma growing on the falx and compressing the motor strip can lead to bilateral leg weakness in the absence of a spinal cord lesion. Meningiomas of the foramen magnum may produce a subtly progressive sequence of ipsilateral arm then leg weakness, which is followed by contralateral leg and arm weakness and may be confused with multiple sclerosis. Seizures are present in approximately 30% of patients who are diagnosed with an intracranial meningioma.113 The risk of seizure is higher in association with non-skull base location, such as convexity or falcine, and tumors associated with peritumoral edema.
Central nervous system
Published in A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha, Clark’s Procedures in Diagnostic Imaging: A System-Based Approach, 2020
A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha
The cerebellum is situated in the posterior cranial fossa behind the pons and the medulla (Fig. 11.2c). It consists of two hemispheres joined by a narrow median strip, termed the vermis. The grey matter lies on the surface and its internal structure forms a branch-like pattern known as the arbor vitae. Cerebellar functions are below the level of consciousness and include the maintenance of balance and posture and co-ordination of voluntary muscle movement.
Posterior fossa morphometry in 170 South Asian children and adults with Chiari malformation and its correlation with tonsillar descent
Published in British Journal of Neurosurgery, 2022
Bijesh Ravindran Nair, Vedantam Rajshekhar
Chiari malformation type 1(CM1) is characterized by various morphometric abnormalities resulting from a smaller posterior cranial fossa (PCF) and overcrowding of the neural structures. Neurological dysfunction occurs due to inferior displacement of the cerebellar tonsils causing hindbrain compression and hydrosyringomyelia. It is hypothesised that CM1 is primarily a mesodermal developmental anomaly, based on experimental observations of vitamin A-induced occipital bone undergrowth and cerebellar displacement in rodents.1 Various morphometric studies have confirmed the occurrence of hypoplastic PCF and normally developed hindbrain structures in CM1.2–11 Basilar invagination (BI) is often associated with CM1, and is seen in 5–13.6% of CM1 patients.5,6,10 However, most morphometric studies do not compare the posterior fossa morphology in patients with and without BI.
Behavioral, histopathological, and biochemical evaluations on the effects of cinnamaldehyde, naloxone, and their combination in morphine-induced cerebellar toxicity
Published in Drug and Chemical Toxicology, 2022
Soraya Mahmoudi, Amir Abbas Farshid, Esmaeal Tamaddonfard, Mehdi Imani, Farahnaz Noroozinia
Cerebellum is situated in posterior cranial fossa and is divided into three major rejoins: flocculonodular lobe, vermis, and two hemispheres (Stoodley and Schmahmann 2018). This structure of the brain has various connections with spinal cord, brain stem, and subcortical and cortical areas and through a variety of neurotransmitters such as acetylcholine, dopamine, and serotonin mediates motor coordination, memory and learning, and pain processing (D’Angelo 2018). Cerebellar lesion may lead to cerebellar ataxia characterized by motor impairments, postural instability, and gait abnormality (Marsden 2018). For example, motor coordinations recorded by balance beam and open field tests have been found to be impaired after experimentally cerebellar hemorrhage induced by intra-cerebellum microinjection of collagenase type VII (Lekic et al. 2011).
Chiari I malformation in children with transverse myelitis
Published in Developmental Neurorehabilitation, 2018
Sathya Vadivelu, Sudhakar Vadivelu, Maureen Mealy, Smurti Patel, Libby Kosnik-Infinger, Daniel Becker
Chiari malformations (CMs) are classically characterized by a peg-like appearance of the cerebellar tonsils and the downward displacement of the posterior cranial fossa contents into the spinal canal.3,13,14 CMs have been divided into two distinct groups based on the degree of herniation. CM type I represents herniation of the cerebellar tonsils and CM type II displays herniation of the fourth ventricle and the medulla oblongata as well as the caudal part of the cerebellar tonsils.15 CMII is exclusively seen in patients with a neural tube defect such as myelomeningocele. At least 5 mm of downward displacement below the foramen magnum is needed to characterize CMI, though the degree of acceptable tonsillar ectopia varies based on age.15–17 CMI is the most common form of CM and may be congenital or acquired in etiology.16 Congenital CMI may be asymptomatic and present only as an incidental finding. However, if symptoms occur, CMI may present with headache, occipital pain, cough-induced pain, ataxia, apnea, and/or sensory or motor changes.18 Less common than congenital, CMI may be acquired and may present as the result of increased intracranial pressure or CSF hypotension.16 Reported prevalence of CMI varies, ranging between .60% and 1.0%.18–22 In a retrospective cohort study performed by Strahle et al., a prevalence of CMI was reported to be as high as 3.6% in the general pediatric population.