HCL-V differs from classic HCL principally in these respects:

Higher white blood cell counts, sometimes exceeding 100,000 cells per microliter
A more aggressive course of disease requiring more frequent treatment
Hairy cells with an unusually large nucleolus for their size
Production of little excess fibronectin produced by classic hairy cells to interfere with bone marrow biopsies
Low or no cell-surface expression of CD25 (interleukin-2 [IL-2] receptor alpha chain, or p55).Low levels of CD25, a part of the receptor for a key immunoregulating hormone, may explain why HCL-V cases are generally much more resistant to treatment by immune-system hormones.HCL-V, which usually features a high proportion of hairy cells without a functional p53 tumor suppressor gene, is somewhat more likely to transform into a higher-grade malignancy. A typical transformation rate of 5-6% has been postulated in the UK, similar to the Richters transformation rate for splenic lymphoma with villous lymphocytes (SLVL) and CLL. Among HCL-V patients, the most aggressive cases normally have the least amount of p53 gene activity. Hairy cells without the p53 gene tend, over time, to displace the less aggressive p53(+) hairy cells. Some evidence suggests that a rearrangement of the immunoglobulin gene VH4-34, which is found in about 40% of HCL-V patients and 10% of classic HCL patients, may be a more important poor prognostic factor than variant status, with HCL-V patients without the VH4-34 rearrangement responding about as well as classic HCL patients. Hairy cell leukemia-Japanese variant
The variant called hairy cell leukemia-Japanese variant, or HCL-J, is more easily treated. Treatment with cladribine has been reported.
Familial hemiplegic migraine (FHM) is an autosomal dominant type of hemiplegic migraine that typically includes weakness of half the body which can last for hours, days, or weeks. It can be accompanied by other symptoms, such as ataxia, coma, and paralysis. Migraine attacks may be provoked by minor head trauma. Some cases of minor head trauma in patients with hemiplegic migraine can develop into delayed cerebral edema, a life-threatening medical emergency. Clinical overlap occurs in some FHM patients with episodic ataxia type 2 and spinocerebellar ataxia type 6, benign familial infantile epilepsy, and alternating hemiplegia of childhood. Three genetic loci for FHM  are known. FHM1, which accounts for about 50% of FHM patients, is caused by mutations in a gene coding for the P/Q-type calcium channel α subunit, CACNA1A. FHM1 is also associated with cerebellar degeneration. FHM2, which accounts for less than 25% of cases, is caused by mutations in the Na+/K+-ATPase gene ATP1A2. FHM3 is a rare subtype of FHM and is caused by mutations in a sodium channel α-subunit coding gene, SCN1A. These three subtypes do not account for all cases of FHM, suggesting the existence of at least one other locus (FHM4). Also, nonfamilial cases of hemiplegic migraine are seen, termed sporadic hemiplegic migraine. These cases seem to have the same causes as the familial cases and represent de novo mutations. Sporadic cases are also clinically identical to familial cases with the exception of a lack of known family history of attacks.