Papilledema

2019 ◽  
pp. 41-46
Author(s):  
Matthew J. Thurtell ◽  
Robert L. Tomsak

Papilledema is the cardinal clinical sign of increased intracranial pressure. In this chapter, we begin by reviewing the symptoms and signs of increased intracranial pressure. We next review potential causes of increased intracranial pressure, which include intracranial masses, obstruction of the ventricular system, obstruction of cerebral venous outflow, decrease in cerebrospinal fluid absorption, increase in cerebrospinal fluid secretion, cerebral edema, medications, and idiopathic intracranial hypertension. We then review the approach to the diagnostic evaluation of increased intracranial pressure, including the recommended neuroimaging studies and cerebrospinal fluid evaluation. Lastly, we discuss the basic management approach for the patient with symptoms and signs of increased intracranial pressure.

2017 ◽  
Author(s):  
Hannah Botfield ◽  
Maria Uldall ◽  
Connar Westgate ◽  
James Mitchell ◽  
Snorre Hagen ◽  
...  

2022 ◽  
Author(s):  
Dagne Barbuskaite ◽  
Eva Kjer Oernbo ◽  
Jonathan Henry Wardman ◽  
Trine Lisberg Toft-Bertelsen ◽  
Eller Conti ◽  
...  

Elevated intracranial pressure (ICP) is observed in many neurological pathologies, e.g. hydrocephalus and stroke. This condition is routinely relieved with neurosurgical approaches, since effective and targeted pharmacological tools are still lacking. The carbonic anhydrase inhibitor, acetazolamide (AZE), may be employed to treat elevated ICP. However, its effectiveness is questioned, its location of action unresolved, and its tolerability low. Here, we employed in vivo and ex vivo approaches to reveal the efficacy and mode of action of AZE in the rat brain. The drug effectively reduced the ICP, irrespective of the mode of drug administration and level of anaesthesia. The effect occurred via a direct action on the choroid plexus and an associated decrease in cerebrospinal fluid secretion, and not indirectly via the systemic action of AZE on renal and vascular processes. Upon a single administration, the reduced ICP endured for approximately 10 h post-AZE delivery with no long-term changes of brain water content or choroidal transporter expression. However, a persistent reduction of ICP was secured with repeated AZE administrations throughout the day. Future specific targeting of choroidal carbonic anhydrases may limit the systemic side effects, and therefore enhance the treatment tolerability and effectiveness in select patient groups experiencing elevated ICP.


2017 ◽  
Vol 645 ◽  
pp. 33-39 ◽  
Author(s):  
Maria Uldall ◽  
Hannah Botfield ◽  
Inger Jansen-Olesen ◽  
Alexandra Sinclair ◽  
Rigmor Jensen

It is generally accepted that meningeal reactions in patients with mumps are due to the direct involvement of the meninges by the mumps virus. With the development of mumps vaccines, this view was extended to vaccinated people, who are considered serious post-vaccine meningitis. In present article, the author states that these reactions are not due to inflammation of the meninges, but to the choroid plexus caused by virulent and vaccine strains. Inflammation leads to an increase in cerebrospinal fluid secretion, which increases intracranial pressure and is manifested by meningeal symptoms. In the presence of this evidence, the author considers that meningeal reactions are not meningitis, but meningisms, based on clinical data, experiments on monkeys and the glymphatic system.


2019 ◽  
Vol 11 (3) ◽  
pp. 295-298
Author(s):  
Amal Alkhotani

Idiopathic intracranial hypertension (IIH) is a syndrome of increased intracranial pressure without a mass lesion or ventriculomegaly and normal cerebrospinal fluid (CSF) composition. Patients typically present with a headache and visual symptoms and signs. Here, we discuss a rare presentation of spontaneous CSF leak secondary to IIH and mild ophthalmic finding that worsened after the cranial repair of the CSF leak.


1981 ◽  
Vol 2 (9) ◽  
pp. 269-276
Author(s):  
John F. Griffith ◽  
Jimmy C. Brasfield

The infant or child with increasing pressure within the cranial cavity must be identified early and treated promptly in order to prevent serious complications or death. When the pressure elevation is gradual it is frequently well tolerated, and the patient may seem deceptively well. There is a critical point, however, beyond which any further increase in pressure leads to a catastrophic deterioration in the patient's condition.1 When this occurs, the outlook for quality survival is poor despite the best therapy. Unfortunately, this can occur when the underlying process is benign and would have been reversible if recognized and treated promptly. For prompt recognition and treatment, the physician must be familiar with the pathophysiology of raised intracranial pressure. PATHOPHYSIOLOGY The intracranial compartment contains blood vessels, cerebrospinal fluid (CSF), brain, and leptomeninges which include the rigid dural membranes forming the falx and tentorium. Whenever there is an increase in the volume of any one of these intracranial components (brain, CSF, blood) there must be a corresponding reduction in the size of the others in order for the intracranial pressure to remain normal. This type of compensation or buffering capacity is particularly important in the early stages of intracranial disease. As the pressure mounts from any type of mass lesion, the CSF is displaced caudally into the spinal subarachnoid space and there is a corresponding increase in the rate of absorption of CSF.2


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